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Volume 26,Issue 11,2019 Table of Contents
2019, 26(11):1181-1188.
DOI: 10.3872/j.issn.1007-385X.2019.11.001
Abstract:
Cancer-associated fibroblasts (CAFs) are one of the major cellularcomponents in tumor microenvironment (TME), which play an important role in cancer progression. MicroRNAs (miRNAs) could participate in the process of CAFs, transformation and metabolism reprogramming, affect the stemness of CAFs, and regulate CAFs-mediated tumor cell proliferation, invasion and chemotherapy resistance; and studies have shown that miRNAs play an important role in CAFs formation and the regulation of CAFs on tumors.The miRNAs released by CAFs can be used as reference indicators for tumor diagnosis, prognosis and drug selection. Thus, exploring the role of miRNAs in the interaction between CAFs and tumor cells and underlining the mechanism, is of great significancefor understanding the occurrence and development of tumors, as well as providing novel strategy for cancer treatment. This review will summarize the role of miRNAs in the formation of CAFs and the regulation of CAFs on tumor cells.
Cancer-associated fibroblasts (CAFs) are one of the major cellularcomponents in tumor microenvironment (TME), which play an important role in cancer progression. MicroRNAs (miRNAs) could participate in the process of CAFs, transformation and metabolism reprogramming, affect the stemness of CAFs, and regulate CAFs-mediated tumor cell proliferation, invasion and chemotherapy resistance; and studies have shown that miRNAs play an important role in CAFs formation and the regulation of CAFs on tumors.The miRNAs released by CAFs can be used as reference indicators for tumor diagnosis, prognosis and drug selection. Thus, exploring the role of miRNAs in the interaction between CAFs and tumor cells and underlining the mechanism, is of great significancefor understanding the occurrence and development of tumors, as well as providing novel strategy for cancer treatment. This review will summarize the role of miRNAs in the formation of CAFs and the regulation of CAFs on tumor cells.
2019, 26(11):1189-1195.
DOI: 10.3872/j.issn.1007-385X.2019.11.002
Abstract:
Objective: To explore the role of Thy-1 cell surface antigen（Thy-1）in promoting epithelial-mesenchymal transition (EMT) in liver cancer HepG2 and MHCC-97 cells by regulating Notch1 pathway. Methods: MHCC-97 cells with high metastatic characteristics and HepG2 cells with low metastatic characteristics were selected as subjects. WB was used to detect the expression levels of Thy-1 and Notch1 in cells. MHCC-97 and HepG2 cells were transfected with lentivirus to construct cells with high and low expression of Thy-1 protein. Cells were treated with Notch1 agonist rhNF-κB (1 gsu/ml) and Notch1 inhibitor MW167 (100 μmol/L) for 24 h respectively. Transwell assay was used to detect the effect of Thy-1 expression on cell invasion; qPCR was used to detect the effect on Notch1 mRNA expression; WB was used to detect the effect on intracellular EMT-related protein expression. Results: The expression levels of Thy-1 and Notch1 in MHCC-97 cells were higher than those in HepG2 cells (P<0.05). Thy-1 overexpressing HepG2 cells and Thy-1 low expressing MHCC-97 cells were successfully constructed. Compared with HepG2 cells, the invasion ability of Thy-1 overexpressing HepG2 cells was significantly enhanced (183.23±55.34 vs 475.78±80.37, P<0.05), vimentin expression was significantly increased (P<0.05), epithelial cadherin protein expression was significantly decreased (P<0.05), and the expression level of Notch1 mRNA was significantly increased (P<0.05). Compared with MHCC-97 cells, the invasion ability of Thy-1 silenced MHCC-97 cells was significantly decreased (543.56±77.94 vs 237.44±62.18, P<0.05), the expression of vimentin was significantly decreased (P<0.05), epithelial cadherin protein expression was significantly increased (P<0.05), and Notch1 mRNA expression level was significantly decreased (P<0.05). Treatment of liver cancer cells with Notch1 activators or inhibitors can reverse the changes caused by Thy-1 silencing or overexpression. Conclusion: Thy-1 can affect the EMT process of HepG2 and MHCC-97 cells by regulating the expression of Notch1.
Objective: To explore the role of Thy-1 cell surface antigen（Thy-1）in promoting epithelial-mesenchymal transition (EMT) in liver cancer HepG2 and MHCC-97 cells by regulating Notch1 pathway. Methods: MHCC-97 cells with high metastatic characteristics and HepG2 cells with low metastatic characteristics were selected as subjects. WB was used to detect the expression levels of Thy-1 and Notch1 in cells. MHCC-97 and HepG2 cells were transfected with lentivirus to construct cells with high and low expression of Thy-1 protein. Cells were treated with Notch1 agonist rhNF-κB (1 gsu/ml) and Notch1 inhibitor MW167 (100 μmol/L) for 24 h respectively. Transwell assay was used to detect the effect of Thy-1 expression on cell invasion; qPCR was used to detect the effect on Notch1 mRNA expression; WB was used to detect the effect on intracellular EMT-related protein expression. Results: The expression levels of Thy-1 and Notch1 in MHCC-97 cells were higher than those in HepG2 cells (P<0.05). Thy-1 overexpressing HepG2 cells and Thy-1 low expressing MHCC-97 cells were successfully constructed. Compared with HepG2 cells, the invasion ability of Thy-1 overexpressing HepG2 cells was significantly enhanced (183.23±55.34 vs 475.78±80.37, P<0.05), vimentin expression was significantly increased (P<0.05), epithelial cadherin protein expression was significantly decreased (P<0.05), and the expression level of Notch1 mRNA was significantly increased (P<0.05). Compared with MHCC-97 cells, the invasion ability of Thy-1 silenced MHCC-97 cells was significantly decreased (543.56±77.94 vs 237.44±62.18, P<0.05), the expression of vimentin was significantly decreased (P<0.05), epithelial cadherin protein expression was significantly increased (P<0.05), and Notch1 mRNA expression level was significantly decreased (P<0.05). Treatment of liver cancer cells with Notch1 activators or inhibitors can reverse the changes caused by Thy-1 silencing or overexpression. Conclusion: Thy-1 can affect the EMT process of HepG2 and MHCC-97 cells by regulating the expression of Notch1.
2019, 26(11):1196-1202.
DOI: 10.3872/j.issn.1007-385X.2019.11.003
Abstract:
Objective: To study the effect of anti-aging Klotho protein on immune escape mediated by regulatory T cells (Treg)/helper T cells 17 (TH17) in mice bearing cervical cancer and its mechanism. Methods: The model of cervical cancer-bearing mice were established,and the control group (normal mice), model group (cervical cancer-bearing mice model), and Klotho treatment group (cervical cancer-bearing mice treated with Klotho protein, 200 ng/d) were set up. The weight of cervical cancer tumors in mice of each group was weighed at 7 and 14 days after treatment respectively, PBMCs were separated at the same time. Flow cytometry was used to detect the changes of T lymphocyte function and the proportion of Treg and TH17 cells in mice. qPCR was used to detect the expressions of Foxp3 and RORγt, the key transcription factors of Treg/TH17 cells, in PBMCs of mice in each group. The changes of IL-17, IL-6, IL-10, TGF-β and IL-23 in PBMCs were detected by ELISA. The protein expressions of Klotho, TGF-β, Foxp3 and RORγt in PBMCs of mice were detected by WB assay. Results: On the 14th day, the tumor inhibition rate of the cervical cancer-bearing mice in the Klotho group was significantly higher than that in the Model group [(52.16±8.25)% vs (23.33±6.29)% the model group to be supplemented, P<0.05). Compared with the Control group, the ratios of Treg and TH17 cells in the lymphocytes of the tumor-bearing mice significantly increased (all P<0.05), the ratios of total T lymphocytes (CD3+ ), auxiliary / induced T lymphocytes (CD3+CD4+ ) and immune index (CD3+CD4+/CD3+CD8+ cells) decreased significantly (all P<0.05); in addition, the mRNA expressions of Foxp3 and RORγt genes, cytokines of IL-17, IL-6, IL-10, TGF-β and IL-23, as well as protein expressions of TGF-β1, Foxp3 and RORγt increased significantly (all P<0.05), while the level of Klotho protein significantly decreased in Model group (P<0.05). Compared with the Model group, the above indicators showed opposite changes in Klotho group (P<0.05), but there was no significant difference with the Control group (all P>0.05). Conclusion: Klotho protein may inhibit Treg/TH17 cell-mediated immune evasion in cervical cancer-bearing mice by inhibiting TGF-β1/Foxp3/RORγt signaling pathway and exert anti-tumor effect.
Objective: To study the effect of anti-aging Klotho protein on immune escape mediated by regulatory T cells (Treg)/helper T cells 17 (TH17) in mice bearing cervical cancer and its mechanism. Methods: The model of cervical cancer-bearing mice were established,and the control group (normal mice), model group (cervical cancer-bearing mice model), and Klotho treatment group (cervical cancer-bearing mice treated with Klotho protein, 200 ng/d) were set up. The weight of cervical cancer tumors in mice of each group was weighed at 7 and 14 days after treatment respectively, PBMCs were separated at the same time. Flow cytometry was used to detect the changes of T lymphocyte function and the proportion of Treg and TH17 cells in mice. qPCR was used to detect the expressions of Foxp3 and RORγt, the key transcription factors of Treg/TH17 cells, in PBMCs of mice in each group. The changes of IL-17, IL-6, IL-10, TGF-β and IL-23 in PBMCs were detected by ELISA. The protein expressions of Klotho, TGF-β, Foxp3 and RORγt in PBMCs of mice were detected by WB assay. Results: On the 14th day, the tumor inhibition rate of the cervical cancer-bearing mice in the Klotho group was significantly higher than that in the Model group [(52.16±8.25)% vs (23.33±6.29)% the model group to be supplemented, P<0.05). Compared with the Control group, the ratios of Treg and TH17 cells in the lymphocytes of the tumor-bearing mice significantly increased (all P<0.05), the ratios of total T lymphocytes (CD3+ ), auxiliary / induced T lymphocytes (CD3+CD4+ ) and immune index (CD3+CD4+/CD3+CD8+ cells) decreased significantly (all P<0.05); in addition, the mRNA expressions of Foxp3 and RORγt genes, cytokines of IL-17, IL-6, IL-10, TGF-β and IL-23, as well as protein expressions of TGF-β1, Foxp3 and RORγt increased significantly (all P<0.05), while the level of Klotho protein significantly decreased in Model group (P<0.05). Compared with the Model group, the above indicators showed opposite changes in Klotho group (P<0.05), but there was no significant difference with the Control group (all P>0.05). Conclusion: Klotho protein may inhibit Treg/TH17 cell-mediated immune evasion in cervical cancer-bearing mice by inhibiting TGF-β1/Foxp3/RORγt signaling pathway and exert anti-tumor effect.
2019, 26(11):1203-1208.
DOI: 10.3872/j.issn.1007-385X.2019.11.004
Abstract:
Objective: To study the effect of ipilimumab on T lymphocytes and Bcl-2 mRNA expression in lung cancer-bearing mice by inhibiting TGF-β1/ERK signaling pathway. Methods: Forty-five C57 mices inoculated with Lewis lung cancer cells were randomly divided into control group, low dose ipilimumab group and high dose ipilimumab group with 15 mice in each. The low and high dose groups were given 3 mg/kg and 5 mg/kg ipilimumab respectively, while the control group was given 0.9% sodium chloride solution with the same volume. The effects of ipilimumab on TGF-β1/ERK signaling pathway, Bcl-2 mRNA expression, immune function improvement and tumor inhibition in three groups were detected by WB and qPCR. Results: After administration of ipilimumab, the tumor weight and volume of mice in low-dose and high-dose groups were significantly lower than that of the control group, and the tumor inhibition rate increased in a dose-dependent manner (P<0.05). The thymus index and spleen index of mice were significantly higher than that of control group, which also increased in a dose-dependent manner (P<0.05). The levels of CD3+, CD4+, CD4+/CD8+ cells in the high and low dose groups were significantly higher than those in the control group, with significantly higher levels in high dose group compared with the low dose group (P<0.05). The levels of serum inflammatory factors were significantly lower than those in control group, and the levels of serum TNF-α, IL-6 and IL-3 in the high dose group were significantly lower than those in the low dose group (P<0.05). The expressions of TGF-β1, ERK1/2, p-ERK1/2 and MEK in tumor tissues of both high and low dose groups significantly decreased, with more lower levels in high dose group than in low dose groups (all P<0.05), and the positive rate of TGF-β1 ex-pression in high dose group was the lowest. The mRNA expression of Bcl-2 in tumor tissues of high and low dose groups decreased significantly after drug administration, with a significantly lower level in high does group than that in low dose group (P<0.05). Conclusion:Ipilimumab can effectively inhibit TGF-β1/ERK signaling pathway, improve immune function and down-regulate the expression of Bcl-2, thus inhibit the growth of Lewis lung cancer cells and play an antitumor role in mice.
Objective: To study the effect of ipilimumab on T lymphocytes and Bcl-2 mRNA expression in lung cancer-bearing mice by inhibiting TGF-β1/ERK signaling pathway. Methods: Forty-five C57 mices inoculated with Lewis lung cancer cells were randomly divided into control group, low dose ipilimumab group and high dose ipilimumab group with 15 mice in each. The low and high dose groups were given 3 mg/kg and 5 mg/kg ipilimumab respectively, while the control group was given 0.9% sodium chloride solution with the same volume. The effects of ipilimumab on TGF-β1/ERK signaling pathway, Bcl-2 mRNA expression, immune function improvement and tumor inhibition in three groups were detected by WB and qPCR. Results: After administration of ipilimumab, the tumor weight and volume of mice in low-dose and high-dose groups were significantly lower than that of the control group, and the tumor inhibition rate increased in a dose-dependent manner (P<0.05). The thymus index and spleen index of mice were significantly higher than that of control group, which also increased in a dose-dependent manner (P<0.05). The levels of CD3+, CD4+, CD4+/CD8+ cells in the high and low dose groups were significantly higher than those in the control group, with significantly higher levels in high dose group compared with the low dose group (P<0.05). The levels of serum inflammatory factors were significantly lower than those in control group, and the levels of serum TNF-α, IL-6 and IL-3 in the high dose group were significantly lower than those in the low dose group (P<0.05). The expressions of TGF-β1, ERK1/2, p-ERK1/2 and MEK in tumor tissues of both high and low dose groups significantly decreased, with more lower levels in high dose group than in low dose groups (all P<0.05), and the positive rate of TGF-β1 ex-pression in high dose group was the lowest. The mRNA expression of Bcl-2 in tumor tissues of high and low dose groups decreased significantly after drug administration, with a significantly lower level in high does group than that in low dose group (P<0.05). Conclusion:Ipilimumab can effectively inhibit TGF-β1/ERK signaling pathway, improve immune function and down-regulate the expression of Bcl-2, thus inhibit the growth of Lewis lung cancer cells and play an antitumor role in mice.
2019, 26(11):1209-1213.
DOI: 10.3872/j.issn.1007-385X.2019.11.005
Abstract:
Objective: To investigate the effect and mechanism of polysaccharide of atractylodes macrocephala (PAM) on the growth of colon cancer cells in mice bearing in-situ colon cancer transplantation tumor. Methods: 1×107 colon cancer HT-29 cells labeled with luciferase were injected into colon serosa of the mice to establish the in-situ colon cancer transplantation tumor model. When the tumor volume reached 230 mm3, the mice were given 30 mg/kg PAM (PAM group) or equal volume of normal saline (Control group) by gavage for 10 consecutive days. The effect of PAM on the growth of colon cancer cells in mice was tested by in vivo tumor imaging technology.The expressions of MHCII and IL-12 in granulocytes, dendritic cells and macrophages, the activation of lymphocytes, and IFN-γ expression in CD4+ and CD8+ cells of tumor tissues were detected by Flow cytometry. Results: PAM significantly inhibited the growth of colon cancer cells in mice bearing in-situ colon cancer transplantation tumor (P<0.01). PAM activated immune cells though increasing the expression levels of MHCII and IL-12 in dendritic cells and macrophages (both P<0.01). PAM significantly increased the frequency of CD8+ cells, NK cells, CD44+/NK cells and CD44+/CD4+ cells in tumor tissues and the number of CD8+ cells and NK cells per unit volume (all P<0.01). PAM significantly increased the IFN-γ secretion of CD4+ and CD8+ cells (both P<0.01), too. Conclusion:PAM inhibits the growth of colon cancer by activating immune cells in tumor tissues of mice bearing in-situ colon cancer transplantation tumor.
Objective: To investigate the effect and mechanism of polysaccharide of atractylodes macrocephala (PAM) on the growth of colon cancer cells in mice bearing in-situ colon cancer transplantation tumor. Methods: 1×107 colon cancer HT-29 cells labeled with luciferase were injected into colon serosa of the mice to establish the in-situ colon cancer transplantation tumor model. When the tumor volume reached 230 mm3, the mice were given 30 mg/kg PAM (PAM group) or equal volume of normal saline (Control group) by gavage for 10 consecutive days. The effect of PAM on the growth of colon cancer cells in mice was tested by in vivo tumor imaging technology.The expressions of MHCII and IL-12 in granulocytes, dendritic cells and macrophages, the activation of lymphocytes, and IFN-γ expression in CD4+ and CD8+ cells of tumor tissues were detected by Flow cytometry. Results: PAM significantly inhibited the growth of colon cancer cells in mice bearing in-situ colon cancer transplantation tumor (P<0.01). PAM activated immune cells though increasing the expression levels of MHCII and IL-12 in dendritic cells and macrophages (both P<0.01). PAM significantly increased the frequency of CD8+ cells, NK cells, CD44+/NK cells and CD44+/CD4+ cells in tumor tissues and the number of CD8+ cells and NK cells per unit volume (all P<0.01). PAM significantly increased the IFN-γ secretion of CD4+ and CD8+ cells (both P<0.01), too. Conclusion:PAM inhibits the growth of colon cancer by activating immune cells in tumor tissues of mice bearing in-situ colon cancer transplantation tumor.
2019, 26(11):1214-1221.
DOI: 10.3872/j.issn.1007-385X.2019.11.006
Abstract:
Objective：To analyze the expression and clinic significance of activity-dependent neuroprotective protein (ADNP) in bladder urothelial carcinoma. Methods: A total of 28 pairs of bladder cancer tissues and corresponding adjacent normal tissuesthat surgically resected at the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University from June 1, 2019 to July 15,2019 were collected for this study. The mRNA expression of ADNP in 20 pairs of tissue samples was detected by qPCR, and the protein expressionin the other 8 pairs was detected by WB. Mean while, the clinicopathological data of patients with bladder urothelial carcinoma treated in our hospital from January 1, 2005 to December 31, 2007 were retrospectively analyzed; and the expression of ADNP in the corresponding paraffin tumor sections were determined with immunohistochemical staining, and normal bladder tissue sections from patients who underwent surgery for other bladder diseases during the same period were collected for comparison. Chi-square test was used to analyze the correlation between ADNP expression and different clinicopathological features, Kaplan-Meier method was used for survival analysis, and Cox risk regression model was used for univariate and multivariate analysis of prognostic factors. Results:The transcriptional and translational levels ofADNPin cancer tissues were higher than those in adjacent normal tissues (all P<0.05), and the expression level of ADNP was correlated with the histological grade, clinical stages and survival status of patients with bladder cancer (P<0.05). Of all the 221 patients included in the study, 32 patients lost to follow-up,and patients with high ADNP expression had poor prognosis (5-year OS: 49.5% vs 78.6%, P<0.01; 5-year PFS: 40.0% vs 72.2%, P<0.01; 10-year OS: 26.6% vs 58.6%, P<0.01; 10-year PFS: 25.3% vs 47.9%, P<0.01). Cox univariate regression analysis showed that ADNP expression was closely related to the prognosis of bladder cancer (P<0.05); and Cox multivariate regression analysisalso showed that ADNP expression (95% CI: 1.300-2.905, P=0.001) was an independent risk factor for the prognosis of bladder cancer. Conclusion: The expression level of ADNP in bladder cancertissuesis significantly higher than that in non-tumor bladder tissues. Histological grade and clinical stageare correlated with the expression level of ADNP. The prognosis of bladder cancer patients with low ADNP expression is relatively better compared to patients with high ADNP expression, andADNP is expected to be a candidate target for specific treatment of bladder cancer.
Objective：To analyze the expression and clinic significance of activity-dependent neuroprotective protein (ADNP) in bladder urothelial carcinoma. Methods: A total of 28 pairs of bladder cancer tissues and corresponding adjacent normal tissuesthat surgically resected at the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University from June 1, 2019 to July 15,2019 were collected for this study. The mRNA expression of ADNP in 20 pairs of tissue samples was detected by qPCR, and the protein expressionin the other 8 pairs was detected by WB. Mean while, the clinicopathological data of patients with bladder urothelial carcinoma treated in our hospital from January 1, 2005 to December 31, 2007 were retrospectively analyzed; and the expression of ADNP in the corresponding paraffin tumor sections were determined with immunohistochemical staining, and normal bladder tissue sections from patients who underwent surgery for other bladder diseases during the same period were collected for comparison. Chi-square test was used to analyze the correlation between ADNP expression and different clinicopathological features, Kaplan-Meier method was used for survival analysis, and Cox risk regression model was used for univariate and multivariate analysis of prognostic factors. Results:The transcriptional and translational levels ofADNPin cancer tissues were higher than those in adjacent normal tissues (all P<0.05), and the expression level of ADNP was correlated with the histological grade, clinical stages and survival status of patients with bladder cancer (P<0.05). Of all the 221 patients included in the study, 32 patients lost to follow-up,and patients with high ADNP expression had poor prognosis (5-year OS: 49.5% vs 78.6%, P<0.01; 5-year PFS: 40.0% vs 72.2%, P<0.01; 10-year OS: 26.6% vs 58.6%, P<0.01; 10-year PFS: 25.3% vs 47.9%, P<0.01). Cox univariate regression analysis showed that ADNP expression was closely related to the prognosis of bladder cancer (P<0.05); and Cox multivariate regression analysisalso showed that ADNP expression (95% CI: 1.300-2.905, P=0.001) was an independent risk factor for the prognosis of bladder cancer. Conclusion: The expression level of ADNP in bladder cancertissuesis significantly higher than that in non-tumor bladder tissues. Histological grade and clinical stageare correlated with the expression level of ADNP. The prognosis of bladder cancer patients with low ADNP expression is relatively better compared to patients with high ADNP expression, andADNP is expected to be a candidate target for specific treatment of bladder cancer.
2019, 26(11):1222-1228.
DOI: 10.3872/j.issn.1007-385X.2019.11.007
Abstract:
Objective: To study the expression and clinical significance of Vimentin and E-cadherin in human breast cancer tissues.Methods: The clinical data of 56 cases of breast cancer patients, who underwent radical mastectomy in Chaohu Hospital Affiliated to Anhui Medical University from January 2014 to January 2016, were retrospectively analyzed. The protein and mRNA expressions of Vimentin and E-cadherin in breast cancer tissues were detected by immunohistochemistry and qPCR, respectively; and the relationship between the expression of Vimentin and E-cadherin in breast cancer tissues and the clinicopathological characteristics was analyzed. Logistic multivariate regression was used to analyze the independent factors affecting the protein expressions of Vimentin and E-cadherin.Spearman was used to analyze the correlation between Vimentin and E-cadherin. Kaplan-Meier was used to analyze the relationship between protein expressions of Vimentin, E-cadherin and prognosis. ROC curve was used to analyze the diagnostic value of Vimentin and E-cadherin on prognosis. Results: The rates of breast cancer tissues with high positive expression of Vimentin and E-cadherin were 76.79% and 19.64%, respectively. Among them, 47 cases (47/56, 83.93%) of breast cancer tissues showed significantly higher Vimentin mRNA expression than adjacent tissues (P<0.05), and 46 cases (46/56, 82.14%) of breast cancer tissues showed significantly lower Ecadherin mRNA expression than adjacent tissues (P<0.05). Vimentin protein expression was associated with tumor size, lymph node metastasis, vascular invasion, histological grade, clinical stage, molecular typing, Ki67+, ER-, PR- and HER2- expression (P<0.05). And E-cadherin protein expression was associated with lymph node metastasis, vascular invasion, histological grade, clinical stage, molecular typing, Ki67+, ER-, PR- and HER2- expression (P<0.05). Tumor size, lymph node metastasis, vascular invasion, histological grading,clinical staging, molecular typing, Ki67+ , ER- , PR- and HER2- expression were all independent factors affecting the expression of Vimentin and E-cadherin (P<0.05). There was a negative correlation between Vimentin and E-cadherin expression (P<0.05). The 3-year survival rate of patients with high expression of Vimentin protein was 67.44%, while that of patients with low expression of E-cadherin protein was 68.89%. Conclusion: The high expression of Vimentin and low expression of E-cadherin in breast cancer tissues may be related to the occurrence, development, invasion and metastasis of breast cancer. It can be used as a reliable indicator of clinical diagnosis and prognosis.
Objective: To study the expression and clinical significance of Vimentin and E-cadherin in human breast cancer tissues.Methods: The clinical data of 56 cases of breast cancer patients, who underwent radical mastectomy in Chaohu Hospital Affiliated to Anhui Medical University from January 2014 to January 2016, were retrospectively analyzed. The protein and mRNA expressions of Vimentin and E-cadherin in breast cancer tissues were detected by immunohistochemistry and qPCR, respectively; and the relationship between the expression of Vimentin and E-cadherin in breast cancer tissues and the clinicopathological characteristics was analyzed. Logistic multivariate regression was used to analyze the independent factors affecting the protein expressions of Vimentin and E-cadherin.Spearman was used to analyze the correlation between Vimentin and E-cadherin. Kaplan-Meier was used to analyze the relationship between protein expressions of Vimentin, E-cadherin and prognosis. ROC curve was used to analyze the diagnostic value of Vimentin and E-cadherin on prognosis. Results: The rates of breast cancer tissues with high positive expression of Vimentin and E-cadherin were 76.79% and 19.64%, respectively. Among them, 47 cases (47/56, 83.93%) of breast cancer tissues showed significantly higher Vimentin mRNA expression than adjacent tissues (P<0.05), and 46 cases (46/56, 82.14%) of breast cancer tissues showed significantly lower Ecadherin mRNA expression than adjacent tissues (P<0.05). Vimentin protein expression was associated with tumor size, lymph node metastasis, vascular invasion, histological grade, clinical stage, molecular typing, Ki67+, ER-, PR- and HER2- expression (P<0.05). And E-cadherin protein expression was associated with lymph node metastasis, vascular invasion, histological grade, clinical stage, molecular typing, Ki67+, ER-, PR- and HER2- expression (P<0.05). Tumor size, lymph node metastasis, vascular invasion, histological grading,clinical staging, molecular typing, Ki67+ , ER- , PR- and HER2- expression were all independent factors affecting the expression of Vimentin and E-cadherin (P<0.05). There was a negative correlation between Vimentin and E-cadherin expression (P<0.05). The 3-year survival rate of patients with high expression of Vimentin protein was 67.44%, while that of patients with low expression of E-cadherin protein was 68.89%. Conclusion: The high expression of Vimentin and low expression of E-cadherin in breast cancer tissues may be related to the occurrence, development, invasion and metastasis of breast cancer. It can be used as a reliable indicator of clinical diagnosis and prognosis.
8 Expression of PD-L1 in triple negative breast cancer tissues and its relationship with angiogenesis
FAN Xiaojie
,
WANG Xinran
,
YUE Meng
,
ZHANG Meng
,
DENG Huiyan
,
GU Lina
,
SANG Meixiang
,
LIU Yueping
2019, 26(11):1229-1234.
DOI: 10.3872/j.issn.1007-385X.2019.11.008
Abstract:
Objective: To investigate the expressions of programmed death ligand 1（PD-L1）in triple-negative breast cancer (TNBC)and its correlation with angiogenesis. Methods: 120 cases of TNBC patients who underwent surgery in the Fourth Hospital of Hebei Medical University from March 1, 2011 to June 1, 2012 were collected. The tumor tissues of patients were surgically resected and confirmed by pathology. PD-L1 protein expression in TNBC tissues of 120 patients was detected by tissue microarray combined with immunohistochemistry,and its relationship with various clinical indicators was analyzed. Blood vessels and lymphatic vessels were labeled withCD34 andD2-40 to detect microvessel density (MVD) and lymphatic vessel density (LVD) in TNBC. Results: The positive expression rate of PD-L1 in the tumor cells and interstitial infiltrating lymphocytes from TNBC was 56.7% (68/120); No correlation was found between PD-L1 protein expression and the gender, age, histological grade, clinical stage, or tumor size of patients with TNBC (P>0.05),but related to the lymph node metastasis (P<0.05) and vascular thrombus (P<0.05). TNBC with high PD-L1 expression exhibited high incidence of lymph node metastasis and formation of vascular thrombus, and the expression of PD-L1 was positively correlated with MVD (r=0.500, P=0.02) as well as LVD (r=0.662, P=0.01). Log-Rank test showed that the survival time of TNBC patients with positive PD-L1 protein expression was significantly shorter than that of patients with negative expression (P<0.05). Cox multivariate analysis suggested that PD-L1 protein expression could be an independent prognostic factor for TNBC overall survival. Conclusion: PD-L1 plays an important role in TNBC angiogenesis and lymphangiogenesis, and is closely related to TNBC invasion and metastasis; blocking PD1/PD-L1 signal pathway is expected to be an effective new strategy for TNBC treatment.
Objective: To investigate the expressions of programmed death ligand 1（PD-L1）in triple-negative breast cancer (TNBC)and its correlation with angiogenesis. Methods: 120 cases of TNBC patients who underwent surgery in the Fourth Hospital of Hebei Medical University from March 1, 2011 to June 1, 2012 were collected. The tumor tissues of patients were surgically resected and confirmed by pathology. PD-L1 protein expression in TNBC tissues of 120 patients was detected by tissue microarray combined with immunohistochemistry,and its relationship with various clinical indicators was analyzed. Blood vessels and lymphatic vessels were labeled withCD34 andD2-40 to detect microvessel density (MVD) and lymphatic vessel density (LVD) in TNBC. Results: The positive expression rate of PD-L1 in the tumor cells and interstitial infiltrating lymphocytes from TNBC was 56.7% (68/120); No correlation was found between PD-L1 protein expression and the gender, age, histological grade, clinical stage, or tumor size of patients with TNBC (P>0.05),but related to the lymph node metastasis (P<0.05) and vascular thrombus (P<0.05). TNBC with high PD-L1 expression exhibited high incidence of lymph node metastasis and formation of vascular thrombus, and the expression of PD-L1 was positively correlated with MVD (r=0.500, P=0.02) as well as LVD (r=0.662, P=0.01). Log-Rank test showed that the survival time of TNBC patients with positive PD-L1 protein expression was significantly shorter than that of patients with negative expression (P<0.05). Cox multivariate analysis suggested that PD-L1 protein expression could be an independent prognostic factor for TNBC overall survival. Conclusion: PD-L1 plays an important role in TNBC angiogenesis and lymphangiogenesis, and is closely related to TNBC invasion and metastasis; blocking PD1/PD-L1 signal pathway is expected to be an effective new strategy for TNBC treatment.
2019, 26(11):1235-1242.
DOI: 10.3872/j.issn.1007-385X.2019.11.009
Abstract:
Objective: To investigate the effects of miR-125a-5p targeting signal transducer and activator of transcription-3 (STAT3)on proliferation and invasion of renal cancer cells, and to preliminarily analyze the action mechanism. Methods: During the period from March 2017 to February 2018, 48 pairs of cancer tissues and corresponding normal adjacent tissues (more than 3 cm away from the tumor margin) resected from patients underwent renal cancer surgery at the Department of Urology, the Air Force Hospital of the Northern War Zone were collected for this study. Normal renal HK-2 cells and renal cancer cells (A498, GRC-1, 786-O and ACHN)were cultured in vitro. The expression of miR-125a-5p in above mentioned tissues and cells was detected by qPCR. miR-125a-5p-NC,miR-125a-5p-mimics, pLV-STAT3 and pLV-STAT3 with miR-125a-5p mimics were transfected into A498 cells, namely NC group (negative control group), miR-125a-5p-mimics group, pLV-STAT3 group and pLV-STAT3+mimics group. The normally cultured A498 cells were used as blank control (Ctrl group). qPCR was performed to detect them RNA expressions of miR-125a-5p and STAT3 in cells of all groups. The bioinformatics prediction software and Dual luciferase assay were performed to analyze the targeting relationship between miR-125a-5p and STAT3. CCK-8, Flow cytometry, Transwell chamber assay were performed to detect cell proliferation activity,apoptosisand invasion, respectively. The expressions of STAT3, Bcl-2, BAX, cleaved cysteinyl aspartate specific proteinase 3 (cl-caspase-3), tumor suppressor gene p21, N-cadherin, E-cadherin, VEGF and HIF-1 in the cells were detected by WB. Results: The expression of miR-125a-5p in renal cancer tissues and cells was significantly lower than that in adjacent normal tissues and normal renal cells (all P<0.05). Compared with NC group, expression of miR-125a-5p in A498 cells transfected with miR-125a-5p-mimics was significantly increased, while expression of STAT3 mRNA was significantly decreased (all P<0.05). STAT3 was the target gene of miR-125a-5p. Compared with NC group, cell viability, number of invasive cells, expressions of Bcl-2, N-cadherin, VEGF, HIF-1, and STAT3 as well as its phosphorylation level in miR-125a-5p mimics group were significantly decreased (all P<0.05), while cell apoptosis and expressions of BAX, p21, cl-caspase-3 and E-cadherin were significantly increased (all P<0.05); the cell viability, number of invasive cells, expressions of Bcl-2, N-cadherin, VEGF, HIF-1 and STAT3 as well as its phosphorylation level in pLV-STAT3 group were significantly increased (all P<0.05), while cell apoptosis and expressions of BAX, p21, cl-caspase-3 and E-cadherin were significantly decreased (all P<0.05). Compared with pLV-STAT3 group, cell viability, number of invasive cells, expressions of Bcl-2, N-cadherin,VEGF, HIF-1, and STAT3 as well asits phosphorylation level were significantly decreased in pLV-STAT3 mimics group (all P<0.05),while cell apoptosis, expressions of BAX, p21, cl-caspase-3 and E-cadherin were significantly increased (all P<0.05). Conclusion: miR-125a-5p shows low expression in renal cancer tissues and cells, which can inhibit proliferation and invasion of A498 cells and promote cell apoptosis by down-regulating its target gene STAT3.
Objective: To investigate the effects of miR-125a-5p targeting signal transducer and activator of transcription-3 (STAT3)on proliferation and invasion of renal cancer cells, and to preliminarily analyze the action mechanism. Methods: During the period from March 2017 to February 2018, 48 pairs of cancer tissues and corresponding normal adjacent tissues (more than 3 cm away from the tumor margin) resected from patients underwent renal cancer surgery at the Department of Urology, the Air Force Hospital of the Northern War Zone were collected for this study. Normal renal HK-2 cells and renal cancer cells (A498, GRC-1, 786-O and ACHN)were cultured in vitro. The expression of miR-125a-5p in above mentioned tissues and cells was detected by qPCR. miR-125a-5p-NC,miR-125a-5p-mimics, pLV-STAT3 and pLV-STAT3 with miR-125a-5p mimics were transfected into A498 cells, namely NC group (negative control group), miR-125a-5p-mimics group, pLV-STAT3 group and pLV-STAT3+mimics group. The normally cultured A498 cells were used as blank control (Ctrl group). qPCR was performed to detect them RNA expressions of miR-125a-5p and STAT3 in cells of all groups. The bioinformatics prediction software and Dual luciferase assay were performed to analyze the targeting relationship between miR-125a-5p and STAT3. CCK-8, Flow cytometry, Transwell chamber assay were performed to detect cell proliferation activity,apoptosisand invasion, respectively. The expressions of STAT3, Bcl-2, BAX, cleaved cysteinyl aspartate specific proteinase 3 (cl-caspase-3), tumor suppressor gene p21, N-cadherin, E-cadherin, VEGF and HIF-1 in the cells were detected by WB. Results: The expression of miR-125a-5p in renal cancer tissues and cells was significantly lower than that in adjacent normal tissues and normal renal cells (all P<0.05). Compared with NC group, expression of miR-125a-5p in A498 cells transfected with miR-125a-5p-mimics was significantly increased, while expression of STAT3 mRNA was significantly decreased (all P<0.05). STAT3 was the target gene of miR-125a-5p. Compared with NC group, cell viability, number of invasive cells, expressions of Bcl-2, N-cadherin, VEGF, HIF-1, and STAT3 as well as its phosphorylation level in miR-125a-5p mimics group were significantly decreased (all P<0.05), while cell apoptosis and expressions of BAX, p21, cl-caspase-3 and E-cadherin were significantly increased (all P<0.05); the cell viability, number of invasive cells, expressions of Bcl-2, N-cadherin, VEGF, HIF-1 and STAT3 as well as its phosphorylation level in pLV-STAT3 group were significantly increased (all P<0.05), while cell apoptosis and expressions of BAX, p21, cl-caspase-3 and E-cadherin were significantly decreased (all P<0.05). Compared with pLV-STAT3 group, cell viability, number of invasive cells, expressions of Bcl-2, N-cadherin,VEGF, HIF-1, and STAT3 as well asits phosphorylation level were significantly decreased in pLV-STAT3 mimics group (all P<0.05),while cell apoptosis, expressions of BAX, p21, cl-caspase-3 and E-cadherin were significantly increased (all P<0.05). Conclusion: miR-125a-5p shows low expression in renal cancer tissues and cells, which can inhibit proliferation and invasion of A498 cells and promote cell apoptosis by down-regulating its target gene STAT3.
2019, 26(11):1243-1248.
DOI: 10.3872/j.issn.1007-385X.2019.11.010
Abstract:
Objective: To explore the molecular mechanism of miR-130a-3p regulating epithelial mesenchymal transition (EMT) to affect the invasion and metastasis of breast cancer cells through HGF/MET pathway. Methods: A total of 22 pairs of cancer tissues and adjacent normal tissues from breast cancer patients, who were admitted to Affiliated Hospital of Chengde Medical College from January 2018 to October 2018, were collected for this study; in addition, breast cancer cell lines (MCF-7, MDA-MB-231 and MDA-MB-453) and normal breast epithelial cells MCF10A were obtained from the Institute of Basic Sciences, Chengde Medical College. And then, the expression of miR-130a-3p in tissues and cell lines were detected by qRT-PCR. The experiment cells were divided into control group, miR-130a-3p mimics group, miR-130a-3p inhibitor group, PHA665752 (a small-molecule MET inhibitor) transfection group and PHA665752+miR-130a-3p inhibitor co-transfection group. CCK-8 assay and Transwell assay were performed to detect the proliferation,invasion and migration of MCF-7 cells, respectively. The expressions of EMT and HGF/MET signaling pathway related proteins in MCF-7 cells were detected by WB. In addition, the targeted relationship between miR-130a-3p and MET was verified by Dual luciferase reporter gene assay. Results: miR-130a-3p was down-regulated in breast cancer tissues and cell lines. Over-expression of miR-130a-3p could suppress the proliferation, invasion, migration and EMT of MCF-7 cells, while knockdown of miR-130a-3p had the opposite results. The results of Dual luciferase reporter gene assay indicated that miR-130a-3p targetedly down-regulated the expression of MET, and miR-130a-3p negatively regulated the expression of HGF/MET signaling pathway. Further experiments confirmed that miR-130a-3p inhibited the proliferation, invasion, migration and EMT of MCF-7 cells by blocking HGF/MET signaling pathway. Conclusion:miR-130a-3p suppresses the EMT of MCF-7 cells via blocking HGF/MET signaling pathway, thereby repressing the invasion and metastasis of MCF-7 cells.
Objective: To explore the molecular mechanism of miR-130a-3p regulating epithelial mesenchymal transition (EMT) to affect the invasion and metastasis of breast cancer cells through HGF/MET pathway. Methods: A total of 22 pairs of cancer tissues and adjacent normal tissues from breast cancer patients, who were admitted to Affiliated Hospital of Chengde Medical College from January 2018 to October 2018, were collected for this study; in addition, breast cancer cell lines (MCF-7, MDA-MB-231 and MDA-MB-453) and normal breast epithelial cells MCF10A were obtained from the Institute of Basic Sciences, Chengde Medical College. And then, the expression of miR-130a-3p in tissues and cell lines were detected by qRT-PCR. The experiment cells were divided into control group, miR-130a-3p mimics group, miR-130a-3p inhibitor group, PHA665752 (a small-molecule MET inhibitor) transfection group and PHA665752+miR-130a-3p inhibitor co-transfection group. CCK-8 assay and Transwell assay were performed to detect the proliferation,invasion and migration of MCF-7 cells, respectively. The expressions of EMT and HGF/MET signaling pathway related proteins in MCF-7 cells were detected by WB. In addition, the targeted relationship between miR-130a-3p and MET was verified by Dual luciferase reporter gene assay. Results: miR-130a-3p was down-regulated in breast cancer tissues and cell lines. Over-expression of miR-130a-3p could suppress the proliferation, invasion, migration and EMT of MCF-7 cells, while knockdown of miR-130a-3p had the opposite results. The results of Dual luciferase reporter gene assay indicated that miR-130a-3p targetedly down-regulated the expression of MET, and miR-130a-3p negatively regulated the expression of HGF/MET signaling pathway. Further experiments confirmed that miR-130a-3p inhibited the proliferation, invasion, migration and EMT of MCF-7 cells by blocking HGF/MET signaling pathway. Conclusion:miR-130a-3p suppresses the EMT of MCF-7 cells via blocking HGF/MET signaling pathway, thereby repressing the invasion and metastasis of MCF-7 cells.
2019, 26(11):1249-1255.
DOI: 10.3872/j.issn.1007-385X.2019.11.011
Abstract:
Objective: To explore the molecular mechanism of miR-17-5p regulating the proliferation and invasion of nasopharyngeal carcinoma cells by regulating the expression of breast cancer metastasis suppressor 1 like (BRMS1-like or BRMS1L) gene. Methods: A total of 40 cases of nasopharyngeal carcinoma tissues and corresponding paracancerous tissues resected from nasopharyngeal carcinoma patients, who were admitted to the General Hospital of Pingdingshan Shenma Medical Group during January 2014 to December 2017, were included in this study; in addition, nasopharyngeal carcinoma cell lines CNE 2, HONE 1, C666-1 and nasopharyngeal immortalized epithelial cell line NP69 were also collected for this study. The expression of miR-17-5p in nasopharyngeal carcinoma tissues and cell lines was detected by qPCR. The targeted relationship between BRMS1L and miR-17-5p was predicted by the StarBase and verified by the Dual luciferase reporter gene assay. Effects of transfection of miR-17-5p mimics and inhibitors on the expression of BRMS1L in CNE2 cells were detected by WB assay. CCK-8, Transwell and Flow cytometry were used to detect the effects of miR-17-5p/BRMS1L axis on the proliferation,migration, invasion and apoptosis of CNE 2 cells. Results: miR-17-5p was highly expressed in nasopharyngeal carcinoma tissues and cell lines (P<0.05 or P<0.01). Knockdown of miR-17-5p significantly inhibited proliferation, invasion and migration of CNE2 cells but promoted apoptosis (P<0.05 or P<0.01); miR-17-5p targeted BRMS1Land down-regulated its expression. Over-expression of BRMS1L significantly inhibited the proliferation, invasion and migration of CNE2 cells but promoted apoptosis (all P<0.01); while simultaneous over-expression of miR-17-5p and BRMS1L reversed the above effects (all P<0.01). Conclusion: miR-17-5p promoted proliferation, invasion, migration and inhibited apoptosis of CNE 2 cells by down-regulating the expression of BRMS1L.
Objective: To explore the molecular mechanism of miR-17-5p regulating the proliferation and invasion of nasopharyngeal carcinoma cells by regulating the expression of breast cancer metastasis suppressor 1 like (BRMS1-like or BRMS1L) gene. Methods: A total of 40 cases of nasopharyngeal carcinoma tissues and corresponding paracancerous tissues resected from nasopharyngeal carcinoma patients, who were admitted to the General Hospital of Pingdingshan Shenma Medical Group during January 2014 to December 2017, were included in this study; in addition, nasopharyngeal carcinoma cell lines CNE 2, HONE 1, C666-1 and nasopharyngeal immortalized epithelial cell line NP69 were also collected for this study. The expression of miR-17-5p in nasopharyngeal carcinoma tissues and cell lines was detected by qPCR. The targeted relationship between BRMS1L and miR-17-5p was predicted by the StarBase and verified by the Dual luciferase reporter gene assay. Effects of transfection of miR-17-5p mimics and inhibitors on the expression of BRMS1L in CNE2 cells were detected by WB assay. CCK-8, Transwell and Flow cytometry were used to detect the effects of miR-17-5p/BRMS1L axis on the proliferation,migration, invasion and apoptosis of CNE 2 cells. Results: miR-17-5p was highly expressed in nasopharyngeal carcinoma tissues and cell lines (P<0.05 or P<0.01). Knockdown of miR-17-5p significantly inhibited proliferation, invasion and migration of CNE2 cells but promoted apoptosis (P<0.05 or P<0.01); miR-17-5p targeted BRMS1Land down-regulated its expression. Over-expression of BRMS1L significantly inhibited the proliferation, invasion and migration of CNE2 cells but promoted apoptosis (all P<0.01); while simultaneous over-expression of miR-17-5p and BRMS1L reversed the above effects (all P<0.01). Conclusion: miR-17-5p promoted proliferation, invasion, migration and inhibited apoptosis of CNE 2 cells by down-regulating the expression of BRMS1L.
12 Effects of long non-coding RNA TUG1 on the proliferation and apoptosis of gastric cancer AGS cells
2019, 26(11):1256-1261.
DOI: 10.3872/j.issn.1007-385X.2019.11.012
Abstract:
Objective: To investigate the expression of lncRNA TUG1 (long non-coding RNA taurine up-regulated gene 1) in gastric cancer and its effect on the proliferation and apoptosis of gastric cancer cells. Methods: Surgically resected gastric cancer tissues and corresponding distal normal tissues (>5 cm away from the margin of tumor) of 40 gastric cancer patients from March 2016 to December 2017 at Ganzhou People's Hospital of Jiangxi Province were collected, and qPCR was used to examine the expression of lncRNA TUG1. AGS gastric cancer cells were transfected with lncRNA TUG1 over-expression plasmids and siRNAs, and the effects of lncRNA TUG1 on cell proliferation and apoptosis were assessed by CCK-8, qPCR and Flow cytometry. Results: lncRNA TUG1 expression was significantly increased in gastric cancer tissues as compared to normal tissues; and it was not correlated with gender, age, tumor size, infiltration depth of tumor, lymph node-metastasis, tumor differentiation and TNM staging. TUG1 over-expression significantly suppressed the expressions of CDKN1A, BAX and Caspase-3 in AGS gastric cancer cells, and decreased G1 phase proportion and apoptosis rate, but increased S phase proportion and cell viability; in contrast, TUG1 siRNA transfection significantly promoted the expressions of CDKN1A, BAX and Caspase-3, and increased G1 phase proportion and apoptosis rate, but decreased S phase proportion and cell viability. Conclusion: Up-regulated lncRNA TUG1 promotes proliferation and inhibits apoptosis of gastric cancer cells.
Objective: To investigate the expression of lncRNA TUG1 (long non-coding RNA taurine up-regulated gene 1) in gastric cancer and its effect on the proliferation and apoptosis of gastric cancer cells. Methods: Surgically resected gastric cancer tissues and corresponding distal normal tissues (>5 cm away from the margin of tumor) of 40 gastric cancer patients from March 2016 to December 2017 at Ganzhou People's Hospital of Jiangxi Province were collected, and qPCR was used to examine the expression of lncRNA TUG1. AGS gastric cancer cells were transfected with lncRNA TUG1 over-expression plasmids and siRNAs, and the effects of lncRNA TUG1 on cell proliferation and apoptosis were assessed by CCK-8, qPCR and Flow cytometry. Results: lncRNA TUG1 expression was significantly increased in gastric cancer tissues as compared to normal tissues; and it was not correlated with gender, age, tumor size, infiltration depth of tumor, lymph node-metastasis, tumor differentiation and TNM staging. TUG1 over-expression significantly suppressed the expressions of CDKN1A, BAX and Caspase-3 in AGS gastric cancer cells, and decreased G1 phase proportion and apoptosis rate, but increased S phase proportion and cell viability; in contrast, TUG1 siRNA transfection significantly promoted the expressions of CDKN1A, BAX and Caspase-3, and increased G1 phase proportion and apoptosis rate, but decreased S phase proportion and cell viability. Conclusion: Up-regulated lncRNA TUG1 promotes proliferation and inhibits apoptosis of gastric cancer cells.
2019, 26(11):1262-1269.
DOI: 10.3872/j.issn.1007-385X.2019.11.013
Abstract:
Objective: To investigate the potential genes associated with lymph nodes metastasis in endometrial cancer (EC) through microarray data analysis and bioinformatics methods. Methods: We screened mRNA expression profiling chip data related to lymph node metastasis of EC from the GEO database and analyzed mRNA expression profile to screen the differentially expressed genes; with the integrated bioinformatics approach, such as biological process annotation, biological signaling pathway enrichment, text mining and protein/gene interactions, we further explored the signaling pathways and genes associated with lymph node metastasis in endometrial cancer. Results: GSE2109 and GSE39099 accessions were obtained in the GEO database, and 8 signaling pathways related to lymph node metastasis in EC (type I interferon, interferon-gamma-mediated, PI3K-Akt, Rap1, TGF-beta, cGMP-PKG, Wnt and Ras) and 14 differentially expressed genes that regulate these pathways were found though the signaling pathways enrichment of common differentially expressed genes. Among them, 11 genes were associated with lymph node metastasis of EC and formed a protein-protein interaction network. PI3K-Akt signaling pathway may be an important signaling pathway for lymph node metastasis in EC. VEGFC and IRS1 may be the important candidate genes related to the regulation of lymph node metastasis in EC. Conclusion: Eight signaling pathways and 11 differentially expressed genes were identified to be associated with lymph node metastasis in EC by bioinformatics analysis.
Objective: To investigate the potential genes associated with lymph nodes metastasis in endometrial cancer (EC) through microarray data analysis and bioinformatics methods. Methods: We screened mRNA expression profiling chip data related to lymph node metastasis of EC from the GEO database and analyzed mRNA expression profile to screen the differentially expressed genes; with the integrated bioinformatics approach, such as biological process annotation, biological signaling pathway enrichment, text mining and protein/gene interactions, we further explored the signaling pathways and genes associated with lymph node metastasis in endometrial cancer. Results: GSE2109 and GSE39099 accessions were obtained in the GEO database, and 8 signaling pathways related to lymph node metastasis in EC (type I interferon, interferon-gamma-mediated, PI3K-Akt, Rap1, TGF-beta, cGMP-PKG, Wnt and Ras) and 14 differentially expressed genes that regulate these pathways were found though the signaling pathways enrichment of common differentially expressed genes. Among them, 11 genes were associated with lymph node metastasis of EC and formed a protein-protein interaction network. PI3K-Akt signaling pathway may be an important signaling pathway for lymph node metastasis in EC. VEGFC and IRS1 may be the important candidate genes related to the regulation of lymph node metastasis in EC. Conclusion: Eight signaling pathways and 11 differentially expressed genes were identified to be associated with lymph node metastasis in EC by bioinformatics analysis.
2019, 26(11):1270-1274.
DOI: 10.3872/j.issn.1007-385X.2019.11.014
Abstract:
基因间的长链非编码RNA-p21（long intergenic non-coding RNA，lincRNA-p21）是lncRNAs中的一种，可通过发挥多种生物学功能影响肿瘤的增殖、转移、侵袭，并且对放、化疗的敏感度产生影响。lincRNA-p21 在胃癌、肝癌、结直肠癌的进展中充当肿瘤抑制基因；也有研究发现lincRNA-p21 在常氧条件下无抑癌作用，而在乏氧条件下能抑制乏氧肿瘤细胞增殖；其能够通过抑制β-连环蛋白信号转导的活性，从而降低肿瘤干细胞的体外活性。因此，lincRNA-p21 有望成为一种新型肿瘤生物标志物，在肿瘤的早期诊断、治疗及预后评估等方面具有重要潜在价值。本文对lincRNA-p21 在消化系统恶性肿瘤中作用的研究进展作一综述
基因间的长链非编码RNA-p21（long intergenic non-coding RNA，lincRNA-p21）是lncRNAs中的一种，可通过发挥多种生物学功能影响肿瘤的增殖、转移、侵袭，并且对放、化疗的敏感度产生影响。lincRNA-p21 在胃癌、肝癌、结直肠癌的进展中充当肿瘤抑制基因；也有研究发现lincRNA-p21 在常氧条件下无抑癌作用，而在乏氧条件下能抑制乏氧肿瘤细胞增殖；其能够通过抑制β-连环蛋白信号转导的活性，从而降低肿瘤干细胞的体外活性。因此，lincRNA-p21 有望成为一种新型肿瘤生物标志物，在肿瘤的早期诊断、治疗及预后评估等方面具有重要潜在价值。本文对lincRNA-p21 在消化系统恶性肿瘤中作用的研究进展作一综述
2019, 26(11):1275-1280.
DOI: 10.3872/j.issn.1007-385X.2019.11.015
Abstract:
细胞穿透肽是一类对细胞膜具有强力穿透作用的短肽，可促进细胞摄取，经细胞穿透肽修饰的脂质体可提高脂质体的入胞率，是目前靶向给药载体研究的新方向。作者查阅了近年来国内外的相关文献，就细胞穿透肽的种类、穿膜机制和细胞穿透肽与多肽、叶酸等大分子组成共修饰脂质体及保护性细胞穿透肽提高对肿瘤细胞的穿透稳定性等在抗肿瘤领域的应用展开综述，以期为脂质体的抗肿瘤靶向给药研究提供参考。
细胞穿透肽是一类对细胞膜具有强力穿透作用的短肽，可促进细胞摄取，经细胞穿透肽修饰的脂质体可提高脂质体的入胞率，是目前靶向给药载体研究的新方向。作者查阅了近年来国内外的相关文献，就细胞穿透肽的种类、穿膜机制和细胞穿透肽与多肽、叶酸等大分子组成共修饰脂质体及保护性细胞穿透肽提高对肿瘤细胞的穿透稳定性等在抗肿瘤领域的应用展开综述，以期为脂质体的抗肿瘤靶向给药研究提供参考。
2019, 26(11):1281-1287.
DOI: 10.3872/j.issn.1007-385X.2019.11.016
Abstract:
肺癌的发病机制非常复杂，目前仍未明确。研究发现miRNA是肿瘤中的一组重要的调节因子，与肺癌的发生发展密切相关，异常表达后可作为致癌miRNA或抑癌miRNA参与调控信号通路基因的表达，影响肺癌细胞的增殖、迁移、侵袭、转移等过程。本文就miRNA作为抑癌或致癌基因在肺癌发生发展中机制的最新研究进展进行综述。
肺癌的发病机制非常复杂，目前仍未明确。研究发现miRNA是肿瘤中的一组重要的调节因子，与肺癌的发生发展密切相关，异常表达后可作为致癌miRNA或抑癌miRNA参与调控信号通路基因的表达，影响肺癌细胞的增殖、迁移、侵袭、转移等过程。本文就miRNA作为抑癌或致癌基因在肺癌发生发展中机制的最新研究进展进行综述。
2019, 26(11):1288-1292.
DOI: 10.3872/j.issn.1007-385X.2019.11.017
Abstract:
口腔鳞状细胞癌是头颈部常见的恶性肿瘤，化疗是其常规治疗手段之一，铂类化疗药物作为一线化疗药物应用于口腔鳞状细胞癌的治疗中。然而化疗耐药极大地限制了铂类化疗药物的临床应用，因此阐明口腔鳞状细胞癌铂类化疗耐药的分子机制具有十分重要的临床意义。本文从药物转运蛋白、DNA损伤修复、细胞凋亡、自噬、上皮间质转化和miRNA等方面综述了口腔鳞状细胞癌铂类化疗耐药的分子机制，以期为逆转铂类耐药及相关肿瘤的生物治疗靶点的开发提供新的思路。
口腔鳞状细胞癌是头颈部常见的恶性肿瘤，化疗是其常规治疗手段之一，铂类化疗药物作为一线化疗药物应用于口腔鳞状细胞癌的治疗中。然而化疗耐药极大地限制了铂类化疗药物的临床应用，因此阐明口腔鳞状细胞癌铂类化疗耐药的分子机制具有十分重要的临床意义。本文从药物转运蛋白、DNA损伤修复、细胞凋亡、自噬、上皮间质转化和miRNA等方面综述了口腔鳞状细胞癌铂类化疗耐药的分子机制，以期为逆转铂类耐药及相关肿瘤的生物治疗靶点的开发提供新的思路。
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.