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Volume 27,Issue 4,2020 Table of Contents
2020, 27(4):341-350.
DOI: 10.3872/j.issn.1007-385X.2020.04.001
Abstract:
Expression and regulation of genetic genes determine the senescent process. Generally, aging has been regarded as an irreversible process. Along with age increasing, each organ of the body including immune system experiences senescence. Immunosenescence promotes the age-related diseases, such as tumor, cardiovascular diseases, Alzheimer's disease, osteoporosis, and so on. These diseases seriously affect the quality of human life and longevity. How to delay senility, maintain immune function, and keep a good health have become the hot points of social concerns. In this review, by discussing the aging, immunosenescence and its related diseases,aging and tumor treatment as well as anti-aging and disease treatment etc, we explore the mechanisms, prevention and treatment of senescence, senescence-related disease and anti-aging.
Expression and regulation of genetic genes determine the senescent process. Generally, aging has been regarded as an irreversible process. Along with age increasing, each organ of the body including immune system experiences senescence. Immunosenescence promotes the age-related diseases, such as tumor, cardiovascular diseases, Alzheimer's disease, osteoporosis, and so on. These diseases seriously affect the quality of human life and longevity. How to delay senility, maintain immune function, and keep a good health have become the hot points of social concerns. In this review, by discussing the aging, immunosenescence and its related diseases,aging and tumor treatment as well as anti-aging and disease treatment etc, we explore the mechanisms, prevention and treatment of senescence, senescence-related disease and anti-aging.
2020, 27(4):351-358.
DOI: 10.3872/j.issn.1007-385X.2020.04.002
Abstract:
Objective: To investigate the relationship between 18F-FDG PET/CT metabolic indicators and expression of immunocyte markers in lung adenocarcinoma patients, and to explore its significance in treatment and prognosis prediction for lung adenocarcinoma patients. Methods: The clinical data of 85 lung adenocarcinoma patients, who admitted to Tianjin Medical University Cancer Institute and Hospital and underwent PET/CT examination from April 2008 to August 2014, were retrospectively analyzed. The expression levels of CD3, CD8, CD68, CD163, CD11c, Foxp3, PD-1 and PD-L1 were determined by immunohistochemistry. Correlations among immune markers (CD68+TAM), PET/CT metabolic parameters (SUVmax, SUVpeak and SUVmean) and tumor metabolic indicators (MTV, TLG)were analyzed using Pearson correlation analysis. The relationships between tumor metabolism, immune indicators and patients’survival outcomes were analyzed using the Kaplan-Meier method. Results: There was a remarkably negative correlation between SUVmax,SUVpeak, SUVmean and expression level of CD68+TAMs (r=-0.253, -0.265, -0.263, all P<0.05) but positive correlation with PD-1+TILs (r=0.427, 0.402, 0.395, all P<0.01) in lung adenocarcinoma patients. MTV and TLG were positively associated with Foxp3+ Tregs and PD-1+ TILs (r=0.313, 0.307, 0.29, 0.407, all P<0.01). Kaplan-Meier survival analysis showed that SUVmax, SUVmean,CD11c+DCs, PD-L1+ cells and TLG were all significantly associated with patients’prognosis (PFS or OS) (all P<0.05). Conclusion:Metabolism of tumor primary lesions is significantly correlated with tumor infiltrating immunocytes, and some of these indicators were associated with patients’prognosis, suggesting that tumor metabolism and microenvironment immune status reflected by 18F-FDG PET/CTindicatorsmay have important reference value for the immunotherapy and prognosis prediction of lung adenocarcinoma patients.
Objective: To investigate the relationship between 18F-FDG PET/CT metabolic indicators and expression of immunocyte markers in lung adenocarcinoma patients, and to explore its significance in treatment and prognosis prediction for lung adenocarcinoma patients. Methods: The clinical data of 85 lung adenocarcinoma patients, who admitted to Tianjin Medical University Cancer Institute and Hospital and underwent PET/CT examination from April 2008 to August 2014, were retrospectively analyzed. The expression levels of CD3, CD8, CD68, CD163, CD11c, Foxp3, PD-1 and PD-L1 were determined by immunohistochemistry. Correlations among immune markers (CD68+TAM), PET/CT metabolic parameters (SUVmax, SUVpeak and SUVmean) and tumor metabolic indicators (MTV, TLG)were analyzed using Pearson correlation analysis. The relationships between tumor metabolism, immune indicators and patients’survival outcomes were analyzed using the Kaplan-Meier method. Results: There was a remarkably negative correlation between SUVmax,SUVpeak, SUVmean and expression level of CD68+TAMs (r=-0.253, -0.265, -0.263, all P<0.05) but positive correlation with PD-1+TILs (r=0.427, 0.402, 0.395, all P<0.01) in lung adenocarcinoma patients. MTV and TLG were positively associated with Foxp3+ Tregs and PD-1+ TILs (r=0.313, 0.307, 0.29, 0.407, all P<0.01). Kaplan-Meier survival analysis showed that SUVmax, SUVmean,CD11c+DCs, PD-L1+ cells and TLG were all significantly associated with patients’prognosis (PFS or OS) (all P<0.05). Conclusion:Metabolism of tumor primary lesions is significantly correlated with tumor infiltrating immunocytes, and some of these indicators were associated with patients’prognosis, suggesting that tumor metabolism and microenvironment immune status reflected by 18F-FDG PET/CTindicatorsmay have important reference value for the immunotherapy and prognosis prediction of lung adenocarcinoma patients.
2020, 27(4):359-364.
DOI: 10.3872/j.issn.1007-385X.2020.04.003
Abstract:
Objective: To investigate the effects and mechanisms of long non-coding RNA (lncRNA) non-coding RNA-activated by DNA damage (NORAD) on the proliferation and migration of esophageal squamous cell carcinoma (ESCC) EC9706 cells. Methods:RT-PCR was used to detect the mRNA expression level of NORAD in different ESCC cells (EC9706, TE1, YES-2, KYSE150). Small interfering RNA (siRNA) targeting NORAD gene was transfected into EC9706 cells (as si-NORAD group) with RNA interference technique to knockdown NORAD expression; in addition, blank control group (as Ctrl group, without any transfection) as well as negative control group (as NC group, transfected with siRNA negative control sequence) were also established. qPCR was used to verify the transfection efficiency. MTT, Colony formation assay and Wound-healing test were used to detect the abilities of proliferation and migration of EC9706 cells before and after NORAD knockdown. Western blotting was used to detect the expressions of E-cadherin,N-cadherin and Snail in EC9706 cells before and after NORAD knockdown. Results: NORAD mRNA was highly expressed in 4 ESCC cell lines. Comparing with TE1, YES-2 and KYSE150 cells, the expression of NORAD mRNA was significantly higher in EC9706 cells (P<0.01). After transfection of NORAD-siRNA into EC9706 cells, the expression of NORAD was down-regulated significantly as comparing with Ctrl group and NC group (all P<0.01), in the meanwhile, the proliferation and migration abilities of EC9706 cells were also significantly suppressed (P<0.05). After NORAD knockdown, the expression of E-cadherin was up-regulated while the expressions of N-cadherin and Snail were down-regulated in EC9706 cells (all P<0.05). Conclusion: NORAD is highly expressed in EC9706 cells;knockdown of NORAD expression can inhibit the proliferation and migration ability of EC9706 probably through up-regulating E-cadherin and down-regulating N-cadherin and Snail.
Objective: To investigate the effects and mechanisms of long non-coding RNA (lncRNA) non-coding RNA-activated by DNA damage (NORAD) on the proliferation and migration of esophageal squamous cell carcinoma (ESCC) EC9706 cells. Methods:RT-PCR was used to detect the mRNA expression level of NORAD in different ESCC cells (EC9706, TE1, YES-2, KYSE150). Small interfering RNA (siRNA) targeting NORAD gene was transfected into EC9706 cells (as si-NORAD group) with RNA interference technique to knockdown NORAD expression; in addition, blank control group (as Ctrl group, without any transfection) as well as negative control group (as NC group, transfected with siRNA negative control sequence) were also established. qPCR was used to verify the transfection efficiency. MTT, Colony formation assay and Wound-healing test were used to detect the abilities of proliferation and migration of EC9706 cells before and after NORAD knockdown. Western blotting was used to detect the expressions of E-cadherin,N-cadherin and Snail in EC9706 cells before and after NORAD knockdown. Results: NORAD mRNA was highly expressed in 4 ESCC cell lines. Comparing with TE1, YES-2 and KYSE150 cells, the expression of NORAD mRNA was significantly higher in EC9706 cells (P<0.01). After transfection of NORAD-siRNA into EC9706 cells, the expression of NORAD was down-regulated significantly as comparing with Ctrl group and NC group (all P<0.01), in the meanwhile, the proliferation and migration abilities of EC9706 cells were also significantly suppressed (P<0.05). After NORAD knockdown, the expression of E-cadherin was up-regulated while the expressions of N-cadherin and Snail were down-regulated in EC9706 cells (all P<0.05). Conclusion: NORAD is highly expressed in EC9706 cells;knockdown of NORAD expression can inhibit the proliferation and migration ability of EC9706 probably through up-regulating E-cadherin and down-regulating N-cadherin and Snail.
2020, 27(4):365-369.
DOI: 10.3872/j.issn.1007-385X.2020.04.004
Abstract:
Objective: To investigate the changes in malignant biological behaviors and expression of programmed cell death-ligand 1 (PD-L1) in esophageal squamous cell carcinoma (ESCC) YES-2 cell line after cis-dichlorodiammine platinum (CDDP) induction (YES-2/CDDP-R). Methods: YES-2 cells were treated with CDDP from low concentration to high concentration (0.25-2.0 μg/ml) with intermittent impact (15-25 days per concentration) to establish ESCC CDDP-resistant cell line YES-2/CDDP-R. The morphological change of YES-2/CDDP-R cells was observed under the inverted microscope. Methyl thiazolyl tetrazolium (MTT) was used to detect cell sensitivity to CDDP. Wound healing assay was used to detect cell migration ability. qPCR and Western blotting were used to detect mRNA and protein expressions of PD-L1. Results: After CDDP gradient treatment for 9 months,YES-2/CDDP-R cells were successfully established. The morphology of the YES-2/CDDP-R cells showed uneven size, intracellular vacuoles and significantly increased black particles along with the appearance of huge cells. The IC50 of CDDP for YES-2/CDDP-R cells was significantly higher than that for parental cells, indicating decreased sensitivity to CDDP (P<0.05). Compared to theYES-2 cells, the proliferation and migration of YES-2/CDDP-R cells were significantly increased (P<0.05 or P<0.01), and the mRNA and protein expressions of PD-L1 were significantly up-regulated (all P<0.001). Conclusion: YES-2 cells with CDDP resistance (YES-2/CDDP-R) were successfully established.The sensitivity of YES-2/CDDP-R cells to CDDP was significantly reduced while the abilities of cell proliferation and migration were enhanced. The up-regulation of PD-L1 in YES-2/CDDP-R cells suggests that CDDP-resistance could promote immune escape by inducing PD-L1 up-regulation.
Objective: To investigate the changes in malignant biological behaviors and expression of programmed cell death-ligand 1 (PD-L1) in esophageal squamous cell carcinoma (ESCC) YES-2 cell line after cis-dichlorodiammine platinum (CDDP) induction (YES-2/CDDP-R). Methods: YES-2 cells were treated with CDDP from low concentration to high concentration (0.25-2.0 μg/ml) with intermittent impact (15-25 days per concentration) to establish ESCC CDDP-resistant cell line YES-2/CDDP-R. The morphological change of YES-2/CDDP-R cells was observed under the inverted microscope. Methyl thiazolyl tetrazolium (MTT) was used to detect cell sensitivity to CDDP. Wound healing assay was used to detect cell migration ability. qPCR and Western blotting were used to detect mRNA and protein expressions of PD-L1. Results: After CDDP gradient treatment for 9 months,YES-2/CDDP-R cells were successfully established. The morphology of the YES-2/CDDP-R cells showed uneven size, intracellular vacuoles and significantly increased black particles along with the appearance of huge cells. The IC50 of CDDP for YES-2/CDDP-R cells was significantly higher than that for parental cells, indicating decreased sensitivity to CDDP (P<0.05). Compared to theYES-2 cells, the proliferation and migration of YES-2/CDDP-R cells were significantly increased (P<0.05 or P<0.01), and the mRNA and protein expressions of PD-L1 were significantly up-regulated (all P<0.001). Conclusion: YES-2 cells with CDDP resistance (YES-2/CDDP-R) were successfully established.The sensitivity of YES-2/CDDP-R cells to CDDP was significantly reduced while the abilities of cell proliferation and migration were enhanced. The up-regulation of PD-L1 in YES-2/CDDP-R cells suggests that CDDP-resistance could promote immune escape by inducing PD-L1 up-regulation.
2020, 27(4):370-376.
DOI: 10.3872/j.issn.1007-385X.2020.04.005
Abstract:
Objective: To investigate the effect of miR-93/EphA4 (Eph receptor A4) axis on the proliferation and migration of nonsmall cell lung cancer (NSCLC) H460 and H1299 cells via regulating extracellular regulated protein kinases (ERK) pathway. Methods:The expression levels of miR-93 in H460 and H1299 cells was detected by qPCR. miR-93 mimics and EphA4 overexpression plasmids were transfected into H460 cells and miR-93 inhibitor was transfected into H1299 cells respectively, after which MTT assay and Transwell assay were used to detect the effects of miR-93 on proliferation and migration of transfected cells. The targeted regulatory relationship between miR-93 and EphA4 was verified by Dual-luciferase reporter gene assay. The expression levels of PCNA (proliferating cell nuclear antigen), EphA4, ERK and p-ERK were detected byWestern blotting. The effects of simultaneous overexpression of miR-93 and EphA4 on proliferation and migration of H460 cells were detected by MTT assay and Transwell assay. Results: The expression of miR-93 in H1299 cells was higher than that in H460 cells (P<0.01). Overexpression of miR-93 promoted proliferation and migration of H460 cells (all P<0.01), and knockdown of miR-93 inhibited proliferation and migration of H1299 cells (all P<0.01). The Dualluciferase reporter gene assay confirmed that miR-93 could target EphA4. Overexpression of miR-93 down-regulated the mRNA and protein expression levels of EphA4 (all P<0.05), and promoted proliferation and migration of H460 cells through targeted regulation of EphA4 and activation of ERK pathway (all P<0.01). Conclusion: miR-93 promotes the proliferation and migration of NSCLC cells,and its mechanism may be related to the targeted regulation of EphA4 and activation of the ERK pathway.
Objective: To investigate the effect of miR-93/EphA4 (Eph receptor A4) axis on the proliferation and migration of nonsmall cell lung cancer (NSCLC) H460 and H1299 cells via regulating extracellular regulated protein kinases (ERK) pathway. Methods:The expression levels of miR-93 in H460 and H1299 cells was detected by qPCR. miR-93 mimics and EphA4 overexpression plasmids were transfected into H460 cells and miR-93 inhibitor was transfected into H1299 cells respectively, after which MTT assay and Transwell assay were used to detect the effects of miR-93 on proliferation and migration of transfected cells. The targeted regulatory relationship between miR-93 and EphA4 was verified by Dual-luciferase reporter gene assay. The expression levels of PCNA (proliferating cell nuclear antigen), EphA4, ERK and p-ERK were detected byWestern blotting. The effects of simultaneous overexpression of miR-93 and EphA4 on proliferation and migration of H460 cells were detected by MTT assay and Transwell assay. Results: The expression of miR-93 in H1299 cells was higher than that in H460 cells (P<0.01). Overexpression of miR-93 promoted proliferation and migration of H460 cells (all P<0.01), and knockdown of miR-93 inhibited proliferation and migration of H1299 cells (all P<0.01). The Dualluciferase reporter gene assay confirmed that miR-93 could target EphA4. Overexpression of miR-93 down-regulated the mRNA and protein expression levels of EphA4 (all P<0.05), and promoted proliferation and migration of H460 cells through targeted regulation of EphA4 and activation of ERK pathway (all P<0.01). Conclusion: miR-93 promotes the proliferation and migration of NSCLC cells,and its mechanism may be related to the targeted regulation of EphA4 and activation of the ERK pathway.
YANG Chunmei
,
ZHANG Lulu
,
HUANG Huakun
,
YUAN Xiaohui
,
ZHANG Ping
,
YE Caihong
,
WEI Mengqi
,
HUANG Yanran
,
LUO Xiaoji
,
LUO Jinyonga
2020, 27(4):377-384.
DOI: 10.3872/j.issn.1007-385X.2020.04.006
Abstract:
Objective: To investigate the effect of alantolactone (ALT) on proliferation, migration, invasion and apoptosis of human osteosarcoma 143B cells and the underlying mechanism. Methods: Osteosarcoma 143B cells were treated with different concentrations of ALT (0, 4, 6, 8, 10 μmol/L). Then, the cell proliferation ability was detected by crystal violet staining and MTT assay, cell migration was determined by Wound-healing test, cell invasion was analyzed by Transwell assay and cell apoptosis rate was detected by Hoechst33258 staining. The mRNA and protein expressions of E-cadherin, N-cadherin, caspase-3, cleaved caspase-3 (c-caspase-3),poly ADP-ribose polymerase (PARP) and cleaved PARP (c-PARP) in 143B cells were detected by qPCR and Western blotting (WB),respectively. TCF/LEF (T cell lymphocyte factor/lymphoid enhancer factor) transcriptional activity was examined with Luciferase reporter gene assay. The mRNA and protein expressions of β -catenin as well as MMP-7 and c-Myc were detected by qPCR and WB,respectively. Results: ALT inhibited proliferation, migration and invasion of osteosarcoma 143B cells and promoted apoptosis (P<0.05 or P<0.01). After the treatment with ALT at 8, 10 μmol/L, the mRNA and protein expressions of E-cadherin and PARP, as well as the protein expressions of c-caspase-3 and c-PARP were up-regulated, while the mRNA and protein expressions of N-cadherin were downregulated (P<0.05 or P<0.01); At the same time, the TCF/LEF transcriptional activity and the mRNAand protein expressions of β-catenin,MMP-7 and c-Myc were significantly down-regulated (P<0.05 or P<0.01). Conclusion: ALT may inhibit the proliferation, migration and invasion and promote cell apoptosis possibly through suppressing Wnt/β-catenin signaling pathway in osteosarcoma 143B cells.
Objective: To investigate the effect of alantolactone (ALT) on proliferation, migration, invasion and apoptosis of human osteosarcoma 143B cells and the underlying mechanism. Methods: Osteosarcoma 143B cells were treated with different concentrations of ALT (0, 4, 6, 8, 10 μmol/L). Then, the cell proliferation ability was detected by crystal violet staining and MTT assay, cell migration was determined by Wound-healing test, cell invasion was analyzed by Transwell assay and cell apoptosis rate was detected by Hoechst33258 staining. The mRNA and protein expressions of E-cadherin, N-cadherin, caspase-3, cleaved caspase-3 (c-caspase-3),poly ADP-ribose polymerase (PARP) and cleaved PARP (c-PARP) in 143B cells were detected by qPCR and Western blotting (WB),respectively. TCF/LEF (T cell lymphocyte factor/lymphoid enhancer factor) transcriptional activity was examined with Luciferase reporter gene assay. The mRNA and protein expressions of β -catenin as well as MMP-7 and c-Myc were detected by qPCR and WB,respectively. Results: ALT inhibited proliferation, migration and invasion of osteosarcoma 143B cells and promoted apoptosis (P<0.05 or P<0.01). After the treatment with ALT at 8, 10 μmol/L, the mRNA and protein expressions of E-cadherin and PARP, as well as the protein expressions of c-caspase-3 and c-PARP were up-regulated, while the mRNA and protein expressions of N-cadherin were downregulated (P<0.05 or P<0.01); At the same time, the TCF/LEF transcriptional activity and the mRNAand protein expressions of β-catenin,MMP-7 and c-Myc were significantly down-regulated (P<0.05 or P<0.01). Conclusion: ALT may inhibit the proliferation, migration and invasion and promote cell apoptosis possibly through suppressing Wnt/β-catenin signaling pathway in osteosarcoma 143B cells.
2020, 27(4):385-390.
DOI: 10.3872/j.issn.1007-385X.2020.04.007
Abstract:
Objective: To investigate the effects of forkhead box transcription factor (FOXK2) overexpression on the proliferation,migration, invasion and adhesion of human ovarian cancer SK-OV-3 cells and its related molecular mechanism. Methods: The open reading frame (ORF) of FOXK2 was cloned into lentivirus expression vector, which was then enveloped in HEK293T cells and transfected into human ovarian cancer SK-OV-3 cells. The overexpression efficiency was detected by qPCR andWestern blotting. The proliferation,migration, invasion and adhesion of SK-OV-3 cells were detected by CCK-8, Scratch-healing, Transwell and Cell adhesion assays respectively, and the expressions of epithelial-mesenchymal transition (EMT) markers were detected by qPCR. Results: The FOXK2 overexpression vector was constructed successfully and packaged into lentivirus, which was then transfected into SK-OV-3 cells. After transfection, the expression of FOXK2 was significantly increased (P<0.01); the proliferation, migration and invasion of SK-OV-3 cells were significantly reduced while the adhesion ability was significantly increased (P<0.05 or P<0.01); and the expression levels of E-cadherin and β-catenin were significantly increased while that of vimentin and fibronection were significantly decreased (all P<0.01). Conclusion: Overexpression of FOXK2 in SK-OV-3 cells leads to a significant decrease in proliferation, migration and invasion but increase in adhesion. The molecular mechanism may be related to the reversion of the EMT process in tumor cells,suggesting that FOXK2 may be a potential target for the diagnosis and treatment of ovarian cancer.
Objective: To investigate the effects of forkhead box transcription factor (FOXK2) overexpression on the proliferation,migration, invasion and adhesion of human ovarian cancer SK-OV-3 cells and its related molecular mechanism. Methods: The open reading frame (ORF) of FOXK2 was cloned into lentivirus expression vector, which was then enveloped in HEK293T cells and transfected into human ovarian cancer SK-OV-3 cells. The overexpression efficiency was detected by qPCR andWestern blotting. The proliferation,migration, invasion and adhesion of SK-OV-3 cells were detected by CCK-8, Scratch-healing, Transwell and Cell adhesion assays respectively, and the expressions of epithelial-mesenchymal transition (EMT) markers were detected by qPCR. Results: The FOXK2 overexpression vector was constructed successfully and packaged into lentivirus, which was then transfected into SK-OV-3 cells. After transfection, the expression of FOXK2 was significantly increased (P<0.01); the proliferation, migration and invasion of SK-OV-3 cells were significantly reduced while the adhesion ability was significantly increased (P<0.05 or P<0.01); and the expression levels of E-cadherin and β-catenin were significantly increased while that of vimentin and fibronection were significantly decreased (all P<0.01). Conclusion: Overexpression of FOXK2 in SK-OV-3 cells leads to a significant decrease in proliferation, migration and invasion but increase in adhesion. The molecular mechanism may be related to the reversion of the EMT process in tumor cells,suggesting that FOXK2 may be a potential target for the diagnosis and treatment of ovarian cancer.
YANG Xiaojun
,
WEI Li
,
ZHENG Xiao
,
XU Bin
,
WANG Qi
,
LIU Yingting
,
ZHANG Dachuan
,
JIANG Jingting
2020, 27(4):391-395.
DOI: 10.3872/j.issn.1007-385X.2020.04.008
Abstract:
Objective: To investigate the expression of chemokine-like factor-like MARVEL transmembrane domain-containing family member 6 (CMTM6) in breast cancer tissues and its correlation with clinicopathological features and prognosis of patients. Methods: A total of 136 breast cancer tissue chips (purchased from Superchip Company), including 42 pairs of matched cancer and paracancerous tissues,were used for this study. The expression level of CMTM6 in cancer and paracancerous tissues was detected by immunohistochemistry. The comparison of CMTM6 expression between breast cancer and paracancerous tissues was conducted by paired χ2 test. The relationship between CMTM6 expression in breast cancer tissues and the clinicopathological characteristics of patients was analyzed by χ2 test. Kaplan-Meier and Log rank test analyses were used to analyze the relationship between CMTM6 expression and the survival of patients, and Cox model was used to evaluate the effect of different indicators on the prognosis of patients. Results: The expression of CMTM6 in breast cancer tissues was significantly higher than that in paracancerous tissues (P<0.01). The expression of CMTM6 was correlated with pathological type of breast cancer and HER2 positivity (P<0.05). The survival time of patients in CMTM6 high expression group was significantly shorter than that of patients in CMTM6 low expression group (P<0.05). Pathological type (HR=10.374, 95%CI: 3.529-30.497, P<0.01), TNM stage (HR=4.599, 95%CI: 1.784-11.856, P<0.01), triple-negative breast cancer (HR=3.370, 95%CI: 1.055-10.761, P<0.05) and high expression of CMTM6 (HR=0.195, 95%CI: 0.073-0.518, P<0.01) were independent risk factors for prognosis of breast cancer patients. Conclusion:CMTM6 is highly expressed in breast cancer tissues, which can be used as a risk factor for prognosis evaluation of breast cancer patients.
Objective: To investigate the expression of chemokine-like factor-like MARVEL transmembrane domain-containing family member 6 (CMTM6) in breast cancer tissues and its correlation with clinicopathological features and prognosis of patients. Methods: A total of 136 breast cancer tissue chips (purchased from Superchip Company), including 42 pairs of matched cancer and paracancerous tissues,were used for this study. The expression level of CMTM6 in cancer and paracancerous tissues was detected by immunohistochemistry. The comparison of CMTM6 expression between breast cancer and paracancerous tissues was conducted by paired χ2 test. The relationship between CMTM6 expression in breast cancer tissues and the clinicopathological characteristics of patients was analyzed by χ2 test. Kaplan-Meier and Log rank test analyses were used to analyze the relationship between CMTM6 expression and the survival of patients, and Cox model was used to evaluate the effect of different indicators on the prognosis of patients. Results: The expression of CMTM6 in breast cancer tissues was significantly higher than that in paracancerous tissues (P<0.01). The expression of CMTM6 was correlated with pathological type of breast cancer and HER2 positivity (P<0.05). The survival time of patients in CMTM6 high expression group was significantly shorter than that of patients in CMTM6 low expression group (P<0.05). Pathological type (HR=10.374, 95%CI: 3.529-30.497, P<0.01), TNM stage (HR=4.599, 95%CI: 1.784-11.856, P<0.01), triple-negative breast cancer (HR=3.370, 95%CI: 1.055-10.761, P<0.05) and high expression of CMTM6 (HR=0.195, 95%CI: 0.073-0.518, P<0.01) were independent risk factors for prognosis of breast cancer patients. Conclusion:CMTM6 is highly expressed in breast cancer tissues, which can be used as a risk factor for prognosis evaluation of breast cancer patients.
2020, 27(4):396-402.
DOI: 10.3872/j.issn.1007-385X.2020.04.009
Abstract:
Objective: To detect the expression of CD39 in head and neck squamous cell carcinoma (HNSCC) tisseus, and to analyze its correlation with patients’clinicopathological features and its prognostic significance. Methods: Tissue specimens and case data of 85 patients with HNSCC underwent surgery at Cancer Hospital of Tianjin from May 2012 to December 2013 were collected for this study. Gene chips were obtained from Oncomine database, and HNSCC cell lines SCC15, UM1, and Cal25 were selected for this study.Online analysis was performed to compare the differential expression of CD39 in buccal mucosa (BM) tissues and HNSCC tissues,Western blotting and Immunohistochemistry (IHC) were used to detect the protein expression of CD39 in HNSCC tissues. Spearman’s correlation analysis was used to study the correlation between the expressions of CD39 and clinicopathological features of HNSCC patients. Both Kaplan-Meier curve analysis and Log rank test were used to analyze the association between the expression of CD39 in HNSCC tissues and the survival of patients, and Cox risk proportional regression model was used to evaluate the relationship between CD39 expression and the risk of relapse. Results: The transcription level of CD39 was obviously up-regulated in HNSCC tissues than in BM tissues (P<0.01), and CD39 expression was detected in HNSCC cell lines SCC15, UM1 and Cal25. Dexamethasone (DXM)could enhance the expression of CD39 in UM1 cells in dose-dependent manner. CD39 was highly expressed in 53 (62.4%) HNSCC patients, which was positively correlated with preoperative chemotherapy (r=0.234, P<0.05). The recurrence-free survival (RFS) of patients with high CD39 expression was significantly shortened (P<0.05), and high CD39 expression was an independent relapse risk factor (HR=2.328, 95%CI=1.091-4.967; P<0.05) for patients with HNSCC. Conclusion: CD39 is DXM-inducively and constitutively expressed in HNSCC. And over-expression of CD39 is an independent predictor of poor prognosis in HNSCC patients, indicating its important role in the progression of HNSCC.
Objective: To detect the expression of CD39 in head and neck squamous cell carcinoma (HNSCC) tisseus, and to analyze its correlation with patients’clinicopathological features and its prognostic significance. Methods: Tissue specimens and case data of 85 patients with HNSCC underwent surgery at Cancer Hospital of Tianjin from May 2012 to December 2013 were collected for this study. Gene chips were obtained from Oncomine database, and HNSCC cell lines SCC15, UM1, and Cal25 were selected for this study.Online analysis was performed to compare the differential expression of CD39 in buccal mucosa (BM) tissues and HNSCC tissues,Western blotting and Immunohistochemistry (IHC) were used to detect the protein expression of CD39 in HNSCC tissues. Spearman’s correlation analysis was used to study the correlation between the expressions of CD39 and clinicopathological features of HNSCC patients. Both Kaplan-Meier curve analysis and Log rank test were used to analyze the association between the expression of CD39 in HNSCC tissues and the survival of patients, and Cox risk proportional regression model was used to evaluate the relationship between CD39 expression and the risk of relapse. Results: The transcription level of CD39 was obviously up-regulated in HNSCC tissues than in BM tissues (P<0.01), and CD39 expression was detected in HNSCC cell lines SCC15, UM1 and Cal25. Dexamethasone (DXM)could enhance the expression of CD39 in UM1 cells in dose-dependent manner. CD39 was highly expressed in 53 (62.4%) HNSCC patients, which was positively correlated with preoperative chemotherapy (r=0.234, P<0.05). The recurrence-free survival (RFS) of patients with high CD39 expression was significantly shortened (P<0.05), and high CD39 expression was an independent relapse risk factor (HR=2.328, 95%CI=1.091-4.967; P<0.05) for patients with HNSCC. Conclusion: CD39 is DXM-inducively and constitutively expressed in HNSCC. And over-expression of CD39 is an independent predictor of poor prognosis in HNSCC patients, indicating its important role in the progression of HNSCC.
2020, 27(4):403-409.
DOI: 10.3872/j.issn.1007-385X.2020.04.010
Abstract:
Objective: To investigate the effect of histone demethylase JMJD3 (jumonji domain-containing protein 3) on the stemness of diffuse large B-cell lymphoma (DLBCL) cells. Methods: The relationship between the expression of JMJD3 and the overall survival of DLBCL patients was analyzed using the clinical data of DLBCL patients in TCGA database. The control plasmid (pCMV) and JMJD3 expression plasmid (pCMV-JMJD3) were transfected into DLBCL cells ofABC and GCB subtype via lipofectamine transfection.Then, the mRNA levels of JMJD3, ALDH1, OCT4 and SOX2 were detected by RT-PCR and qPCR; the activity of ALDH1 enzyme was detected by Flow cytometry; the protein expressions of OCT4 and SOX2 were detected by Western blotting. Gene enrichment in DLBCL patients with high JMJD3 expression was analyzed by gene set enrichment analysis (GSEA). Results: The result of prognosis analysis showed that high expression of JMJD3 was related with poor prognosis in DLBCL patients (P<0.05); however, multivariate analysis showed that the expression of JMJD3 was not the independent factor affecting the prognosis of DLBCL patients (all P>0.05).The expression of JMJD3 was remarkably increased in DLBCL cells transfected with pCMV-JMJD3, which led to significantly increased mRNA level and enzyme activity of ALDH1 as well as up-regulated mRNA and protein expressions of OCT4 and SOX2 (P<0.05 or P<0.01). GSEA analysis showed that enrichment of Wnt/β -catenin signaling pathway related gene set was observed in DLBCL patients with high JMJD3 expression (P<0.05). Conclusion: JMJD3 promotes the stemness of DLBCL cells, which may be a potential therapeutic target for DLBCL patients.
Objective: To investigate the effect of histone demethylase JMJD3 (jumonji domain-containing protein 3) on the stemness of diffuse large B-cell lymphoma (DLBCL) cells. Methods: The relationship between the expression of JMJD3 and the overall survival of DLBCL patients was analyzed using the clinical data of DLBCL patients in TCGA database. The control plasmid (pCMV) and JMJD3 expression plasmid (pCMV-JMJD3) were transfected into DLBCL cells ofABC and GCB subtype via lipofectamine transfection.Then, the mRNA levels of JMJD3, ALDH1, OCT4 and SOX2 were detected by RT-PCR and qPCR; the activity of ALDH1 enzyme was detected by Flow cytometry; the protein expressions of OCT4 and SOX2 were detected by Western blotting. Gene enrichment in DLBCL patients with high JMJD3 expression was analyzed by gene set enrichment analysis (GSEA). Results: The result of prognosis analysis showed that high expression of JMJD3 was related with poor prognosis in DLBCL patients (P<0.05); however, multivariate analysis showed that the expression of JMJD3 was not the independent factor affecting the prognosis of DLBCL patients (all P>0.05).The expression of JMJD3 was remarkably increased in DLBCL cells transfected with pCMV-JMJD3, which led to significantly increased mRNA level and enzyme activity of ALDH1 as well as up-regulated mRNA and protein expressions of OCT4 and SOX2 (P<0.05 or P<0.01). GSEA analysis showed that enrichment of Wnt/β -catenin signaling pathway related gene set was observed in DLBCL patients with high JMJD3 expression (P<0.05). Conclusion: JMJD3 promotes the stemness of DLBCL cells, which may be a potential therapeutic target for DLBCL patients.
2020, 27(4):410-415.
DOI: 10.3872/j.issn.1007-385X.2020.04.011
Abstract:
Objective: To explore the clinical significance of multiple serum cytokines in early diagnosis and progression assessment of gastric adenocarcinoma. Methods: Peripheral blood samples of 85 healthy subjects (healthy control group) and 81 patients with pathologically confirmed gastric adenocarcinoma (gastric cancer group) were collected from November 2017 to February 2018 at Shanxi Cancer Hospital.Serum levels of 17 cytokines (including IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-15, IL-17A, TNF-α, TNF-β, GM-CSF, G-CSF,IFN-γ, IP-10, MCP-1 and VEGF-A) were measured byAimPlex multiplex assay technology. Their diagnostic values were analyzed by receiver operating characteristic (ROC) curve. Results: Serum levels of IL-10, IL-8, IL-6, IP-10, MCP-1, VEGF-A and IL-12p70 were significantly higher in gastric cancer patients than those in healthy controls (all P<0.01). There were significantly increased levels of IL-8, IL-6 and VEGF-Ain advanced-stage gastric cancer (stage I/II) group over early-stage gastric cancer (stage III/IV) group (all P<0.01). AUC (areas under the curve) of IL-8, IL-6, IL-10, IP-10, MCP-1, IL-12p70 and VEGF-A for distinguishing early-stage gastric cancer patients from healthy controls was 0.98, 0.92, 0.89, 0.84, 0.76, 0.74 and 0.58, respectively. The diagnostic sensitivity of IL-8, IL-6 and IL-10 was 97.4%, 89.5% and 97.4%, respectively, and the specificity was 87.1%, 85.9%and 77.6%, respectively. TheAUC of IL-8, IL-6 and VEGF-Afor distinguishing advanced-stage gastric cancer patients from early-stage gastric cancer patients was 0.82, 0.72 and 0.69, respectively. Thediagnosticsensitivity of IL-8, IL-6 and VEGF-A was 83.7%, 60.5% and 41.9%, respectively, and the specificity was 71.1%, 76.3%and 92.1%, respectively.Conclusion: The combined detection of serumIL-8, IL-6 and IL-10 may be a potential approach for early screening of gastric adenocarcinoma,which can also be used to assess the progression of gastric adenocarcinoma.
Objective: To explore the clinical significance of multiple serum cytokines in early diagnosis and progression assessment of gastric adenocarcinoma. Methods: Peripheral blood samples of 85 healthy subjects (healthy control group) and 81 patients with pathologically confirmed gastric adenocarcinoma (gastric cancer group) were collected from November 2017 to February 2018 at Shanxi Cancer Hospital.Serum levels of 17 cytokines (including IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-15, IL-17A, TNF-α, TNF-β, GM-CSF, G-CSF,IFN-γ, IP-10, MCP-1 and VEGF-A) were measured byAimPlex multiplex assay technology. Their diagnostic values were analyzed by receiver operating characteristic (ROC) curve. Results: Serum levels of IL-10, IL-8, IL-6, IP-10, MCP-1, VEGF-A and IL-12p70 were significantly higher in gastric cancer patients than those in healthy controls (all P<0.01). There were significantly increased levels of IL-8, IL-6 and VEGF-Ain advanced-stage gastric cancer (stage I/II) group over early-stage gastric cancer (stage III/IV) group (all P<0.01). AUC (areas under the curve) of IL-8, IL-6, IL-10, IP-10, MCP-1, IL-12p70 and VEGF-A for distinguishing early-stage gastric cancer patients from healthy controls was 0.98, 0.92, 0.89, 0.84, 0.76, 0.74 and 0.58, respectively. The diagnostic sensitivity of IL-8, IL-6 and IL-10 was 97.4%, 89.5% and 97.4%, respectively, and the specificity was 87.1%, 85.9%and 77.6%, respectively. TheAUC of IL-8, IL-6 and VEGF-Afor distinguishing advanced-stage gastric cancer patients from early-stage gastric cancer patients was 0.82, 0.72 and 0.69, respectively. Thediagnosticsensitivity of IL-8, IL-6 and VEGF-A was 83.7%, 60.5% and 41.9%, respectively, and the specificity was 71.1%, 76.3%and 92.1%, respectively.Conclusion: The combined detection of serumIL-8, IL-6 and IL-10 may be a potential approach for early screening of gastric adenocarcinoma,which can also be used to assess the progression of gastric adenocarcinoma.
2020, 27(4):416-419.
DOI: 10.3872/j.issn.1007-385X.2020.04.012
Abstract:
Objective: To investigate the expression of long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) in esophageal squamous cell carcinoma (ESCC) tissues, and to analyze its relationship with clinicopathological features and prognosis of ESCC patients. Methods: The expression of DGCR5 in ESCC data set from TCGA database was analyzed by bioinformatics method. Sixty pairs of ESCC tissues and para-cancerous tissues resected at the Fourth Hospital of Hebei Medical University from August 2016 to March 2017 were collected for this study. The expression of DGCR5 in ESCC tissues was detected by qPCR. The correlation between the expression of DGCR5 and the clinicopathological features and prognosis of ESCC patients was analyzed. Results: TCGA database analysis showed that the expression of DGCR5 in ESCC tissues was significantly higher than that in normal esophageal tissues (P<0.01). The expression of DGCR5 in ESCC tissues was significantly higher than that in para-cancerous tissues (P<0.01). The expression level of DGCR5 was significantly correlated with TNM staging and lymph node metastasis in ESCC patients (all P<0.05). Kaplan-Meier univariate analysis showed that the 2-year survival rate of ESCC patients with high DGCR5 expression was significantly lower than that of patients with low expression (P<0.05). Conclusion: DGCR5 is highly expressed in ESCC tissues and is closely related to TNM staging, lymph node metastasis and poor prognosis, which may serve as a molecular marker for early diagnosis and prognosis prediction of ESCC.
Objective: To investigate the expression of long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) in esophageal squamous cell carcinoma (ESCC) tissues, and to analyze its relationship with clinicopathological features and prognosis of ESCC patients. Methods: The expression of DGCR5 in ESCC data set from TCGA database was analyzed by bioinformatics method. Sixty pairs of ESCC tissues and para-cancerous tissues resected at the Fourth Hospital of Hebei Medical University from August 2016 to March 2017 were collected for this study. The expression of DGCR5 in ESCC tissues was detected by qPCR. The correlation between the expression of DGCR5 and the clinicopathological features and prognosis of ESCC patients was analyzed. Results: TCGA database analysis showed that the expression of DGCR5 in ESCC tissues was significantly higher than that in normal esophageal tissues (P<0.01). The expression of DGCR5 in ESCC tissues was significantly higher than that in para-cancerous tissues (P<0.01). The expression level of DGCR5 was significantly correlated with TNM staging and lymph node metastasis in ESCC patients (all P<0.05). Kaplan-Meier univariate analysis showed that the 2-year survival rate of ESCC patients with high DGCR5 expression was significantly lower than that of patients with low expression (P<0.05). Conclusion: DGCR5 is highly expressed in ESCC tissues and is closely related to TNM staging, lymph node metastasis and poor prognosis, which may serve as a molecular marker for early diagnosis and prognosis prediction of ESCC.
2020, 27(4):420-426.
DOI: 10.3872/j.issn.1007-385X.2020.04.013
Abstract:
Objective: To investigate the influence of glutathione S-transferase P-1 (GSTP1) genetic variation on the recurrence risk and prognosis of colorectal cancer (CRC) patients received postoperative adjuvant chemotherapy. Methods: The clinical data of 195 CRC patients, who received postoperative adjuvant chemotherapy in the Department of Gastroenterology of the First Affiliated Hospital of Zhengzhou University from January 2010 to December 2018, were collected for this study. 5-fluorouracil (5-FU) based adjuvant chemotherapy was given after surgical resection. The recurrence status of the patients was assessed during hospitalization period, and the long-term survival data of patients were obtained by telephone follow-up after finishing the scheduled adjuvant chemotherapy.GSTP1 genotyping was performed with the DNA extracted from peripheral blood specimens, and its correlation with patients’clinical characteristics was analyzed. Additionally, RNAwas extracted from peripheral blood mononuclear cell (PBMC) specimens of some CRC patients that prior to chemotherapy for GSTP1 mRNA expression analysis. The univariate analysis of genotypes and prognosis was carried out by Kaplan-Meier survival analysis, and adjusted by multivariate Cox regression model. Results: The median disease-free survival (DFS) of the 195 CRC patients was 4.8 years, and the median overall survival (OS) was 6.2 years. Polymorphism analysis indicated that the I105Vlocus of GSTP-1 coding region was correlated with prognosis. The prevalence of I105V in the study population:AA genotype of 135 cases (69.23%), AG genotype of 56 cases (28.72%) and GG genotype of 4 cases (2.05%), the minor allele frequency of I105V was 0.16. The genotype distribution was in accordance with Hardy-Weinberg equilibrium (P>0.05). The analysis of recurrence risk and prognosis found that the median DFS of patients with AA genotype and AG/GG genotype was 5.7 and 3.9 years respectively (P<0.01), while the median OS of two groups of patients was 7.0 and 4.5 years respectively (P<0.01). The multivariate Cox regression results indicated that AG/GG genotype was an independent factor for OS (OR=1.54, P<0.05). The mRNA expression of GSTP1 in PBMC of the patients with AG/GG genotypes were significantly higher than those patients with AA genotype (P<0.01).Conclusion: GSTP1 I105V genetic variation influences the recurrence risk and prognosis of CRC patients received postoperative adjuvant chemotherapy possibly via mediating the mRNA expression of GSTP1.
Objective: To investigate the influence of glutathione S-transferase P-1 (GSTP1) genetic variation on the recurrence risk and prognosis of colorectal cancer (CRC) patients received postoperative adjuvant chemotherapy. Methods: The clinical data of 195 CRC patients, who received postoperative adjuvant chemotherapy in the Department of Gastroenterology of the First Affiliated Hospital of Zhengzhou University from January 2010 to December 2018, were collected for this study. 5-fluorouracil (5-FU) based adjuvant chemotherapy was given after surgical resection. The recurrence status of the patients was assessed during hospitalization period, and the long-term survival data of patients were obtained by telephone follow-up after finishing the scheduled adjuvant chemotherapy.GSTP1 genotyping was performed with the DNA extracted from peripheral blood specimens, and its correlation with patients’clinical characteristics was analyzed. Additionally, RNAwas extracted from peripheral blood mononuclear cell (PBMC) specimens of some CRC patients that prior to chemotherapy for GSTP1 mRNA expression analysis. The univariate analysis of genotypes and prognosis was carried out by Kaplan-Meier survival analysis, and adjusted by multivariate Cox regression model. Results: The median disease-free survival (DFS) of the 195 CRC patients was 4.8 years, and the median overall survival (OS) was 6.2 years. Polymorphism analysis indicated that the I105Vlocus of GSTP-1 coding region was correlated with prognosis. The prevalence of I105V in the study population:AA genotype of 135 cases (69.23%), AG genotype of 56 cases (28.72%) and GG genotype of 4 cases (2.05%), the minor allele frequency of I105V was 0.16. The genotype distribution was in accordance with Hardy-Weinberg equilibrium (P>0.05). The analysis of recurrence risk and prognosis found that the median DFS of patients with AA genotype and AG/GG genotype was 5.7 and 3.9 years respectively (P<0.01), while the median OS of two groups of patients was 7.0 and 4.5 years respectively (P<0.01). The multivariate Cox regression results indicated that AG/GG genotype was an independent factor for OS (OR=1.54, P<0.05). The mRNA expression of GSTP1 in PBMC of the patients with AG/GG genotypes were significantly higher than those patients with AA genotype (P<0.01).Conclusion: GSTP1 I105V genetic variation influences the recurrence risk and prognosis of CRC patients received postoperative adjuvant chemotherapy possibly via mediating the mRNA expression of GSTP1.
2020, 27(4):445-451.
DOI: 10.3872/j.issn.1007-385X.2020.04.017
Abstract:
仑伐替尼（lenvatinib）是日本卫材（Eisai）公司研发并生产的一种多靶点酪氨酸激酶抑制剂（tyrosine kinase inhibitor,TKI），可抑制多条影响血管生成和细胞增殖的重要通路，包括血管内皮生长因子受体（vascular endothelial growth factor receptor，VEGFR）1~3、成纤维细胞生长因子受体（fibroblast growth factor receptor，FGFR）1~4、血小板衍生生长因子受体α 及原癌基因RET和KIT。这些信号通路已在之前的研究中被证实与多种恶性肿瘤的发生发展及不良预后相关，仑伐替尼可以通过阻断以上通路发挥抑制肿瘤生长的作用。在目前临床所使用的已知的激酶抑制剂中，仑伐替尼是唯一同时对VEGFR和FGFR有抑制作用的TKI类药物。在一系列临床试验中，仑伐替尼对多种实体瘤的单药治疗效果也得到了进一步的临床证实，与其他药物联合治疗的临床试验也在不断开展。本文论述近年来仑伐替尼在甲状腺癌、肝细胞癌、肾细胞癌、子宫内膜癌、非小细胞肺癌以及恶性黑色素瘤等实体瘤治疗中的研究进展。
仑伐替尼（lenvatinib）是日本卫材（Eisai）公司研发并生产的一种多靶点酪氨酸激酶抑制剂（tyrosine kinase inhibitor,TKI），可抑制多条影响血管生成和细胞增殖的重要通路，包括血管内皮生长因子受体（vascular endothelial growth factor receptor，VEGFR）1~3、成纤维细胞生长因子受体（fibroblast growth factor receptor，FGFR）1~4、血小板衍生生长因子受体α 及原癌基因RET和KIT。这些信号通路已在之前的研究中被证实与多种恶性肿瘤的发生发展及不良预后相关，仑伐替尼可以通过阻断以上通路发挥抑制肿瘤生长的作用。在目前临床所使用的已知的激酶抑制剂中，仑伐替尼是唯一同时对VEGFR和FGFR有抑制作用的TKI类药物。在一系列临床试验中，仑伐替尼对多种实体瘤的单药治疗效果也得到了进一步的临床证实，与其他药物联合治疗的临床试验也在不断开展。本文论述近年来仑伐替尼在甲状腺癌、肝细胞癌、肾细胞癌、子宫内膜癌、非小细胞肺癌以及恶性黑色素瘤等实体瘤治疗中的研究进展。
2020, 27(4):452-456.
DOI: 10.3872/j.issn.1007-385X.2020.04.018
Abstract:
PIWI 蛋白相互作用RNA（PIWI-interacting RNA，piRNA）及PIWI 蛋白通过表观遗传沉默影响肿瘤的发生发展，并与恶性肿瘤的增殖、侵袭、转移和预后不良密切相关，是潜在的新型肿瘤标志物和预后判断因子。卵巢癌是妇科三大恶性肿瘤之一，晚期易复发转移、产生耐药和病死率高，目前仍缺乏有效的早期肿瘤标志物和诊断方法。近年有研究表明，piRNA和PIWI蛋白在卵巢癌中呈异常表达，通过转录后机制参与调控卵巢癌的发生发展。本文主要从piRNA的生物学特性、在肿瘤中表观遗传沉默的相关机制和piRNA 在卵巢癌中的作用及其机制最新研究进展进行综述，为研究早期诊断卵巢癌的分子标志物提供参考依据。
PIWI 蛋白相互作用RNA（PIWI-interacting RNA，piRNA）及PIWI 蛋白通过表观遗传沉默影响肿瘤的发生发展，并与恶性肿瘤的增殖、侵袭、转移和预后不良密切相关，是潜在的新型肿瘤标志物和预后判断因子。卵巢癌是妇科三大恶性肿瘤之一，晚期易复发转移、产生耐药和病死率高，目前仍缺乏有效的早期肿瘤标志物和诊断方法。近年有研究表明，piRNA和PIWI蛋白在卵巢癌中呈异常表达，通过转录后机制参与调控卵巢癌的发生发展。本文主要从piRNA的生物学特性、在肿瘤中表观遗传沉默的相关机制和piRNA 在卵巢癌中的作用及其机制最新研究进展进行综述，为研究早期诊断卵巢癌的分子标志物提供参考依据。
2020, 27(4):457-462.
DOI: 10.3872/j.issn.1007-385X.2020.04.019
Abstract:
外泌体是机体内大多数细胞分泌的具有脂质双层膜的微小膜泡，其广泛分布于各种体液中，通过携带和传递重要的信号分子如miRNA、mRNA、蛋白质等，影响肿瘤的发生发展。外泌体miRNA在肺癌的发生与演进过程中扮演重要角色，通过参与细胞间通信及调控信号通路基因的表达，在肿瘤转移、肿瘤免疫调节、肿瘤耐药及新生血管形成中发挥重要作用。此外，外泌体miRNA可作为肿瘤潜在治疗靶点及早期诊断的生物标志物，为肺癌治疗带来新前景。本文就外泌体miRNA在肺癌发生发展中的功能和作用研究进展进行综述。
外泌体是机体内大多数细胞分泌的具有脂质双层膜的微小膜泡，其广泛分布于各种体液中，通过携带和传递重要的信号分子如miRNA、mRNA、蛋白质等，影响肿瘤的发生发展。外泌体miRNA在肺癌的发生与演进过程中扮演重要角色，通过参与细胞间通信及调控信号通路基因的表达，在肿瘤转移、肿瘤免疫调节、肿瘤耐药及新生血管形成中发挥重要作用。此外，外泌体miRNA可作为肿瘤潜在治疗靶点及早期诊断的生物标志物，为肺癌治疗带来新前景。本文就外泌体miRNA在肺癌发生发展中的功能和作用研究进展进行综述。
2020, 27(4):463-464.
DOI: 10.3872/j.issn.1007-385X.2020.04.020
Abstract:
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- 《中国肿瘤生物治疗杂志》
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.