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Volume 24,Issue 2,2017 Table of Contents
2017, 24(2):103-111.
DOI: 10.3872/j.issn.1007-385X.2017.02.001
Abstract:
Malignant transformation induced by chronic inflammation represents a common process of carcinogenesis for the majority of cancers. Authors presented a novel theory framework of cancer evolution-development (Cancer Evo-Dev) based on the evidence chains from genome researches, somatic mutations/epigenetic alterations-related signaling-pathway studies, and epidemiological investigations. The central contents of this theory include the following aspects: the interactions of genetic predispositions of key immune/inflammatory molecules and environmental exposures induce and maintain the chronic non-resolving inflammation. Under the microenvironment of non-resolving inflammation, cytidine deaminases are persistently trans-activated by proinflammatory factors and bridge chronic inflammation and cancers by promoting the generation of vast somatic mutations. Most mutant cells are eliminated in the hostile inflammatory microenvironments, only a small percentage of the mutant cells undergo de-differentiation to acquire the characteristics of “stem-ness” via altering signaling-pathways by somatic mutations and inflammation-related epigenetic modifications, and develop into cancer initiating cells. This carcinogenic process follows the evolution regulation of “mutation-selection-adaptation”. Cancer Evo-Dev not only facilitates understanding the basic mechanism of inflammation-cancer transformation, but also contributes to the development of specific prophylaxis, prediction, and targeted therapy of cancers.
Malignant transformation induced by chronic inflammation represents a common process of carcinogenesis for the majority of cancers. Authors presented a novel theory framework of cancer evolution-development (Cancer Evo-Dev) based on the evidence chains from genome researches, somatic mutations/epigenetic alterations-related signaling-pathway studies, and epidemiological investigations. The central contents of this theory include the following aspects: the interactions of genetic predispositions of key immune/inflammatory molecules and environmental exposures induce and maintain the chronic non-resolving inflammation. Under the microenvironment of non-resolving inflammation, cytidine deaminases are persistently trans-activated by proinflammatory factors and bridge chronic inflammation and cancers by promoting the generation of vast somatic mutations. Most mutant cells are eliminated in the hostile inflammatory microenvironments, only a small percentage of the mutant cells undergo de-differentiation to acquire the characteristics of “stem-ness” via altering signaling-pathways by somatic mutations and inflammation-related epigenetic modifications, and develop into cancer initiating cells. This carcinogenic process follows the evolution regulation of “mutation-selection-adaptation”. Cancer Evo-Dev not only facilitates understanding the basic mechanism of inflammation-cancer transformation, but also contributes to the development of specific prophylaxis, prediction, and targeted therapy of cancers.
2017, 24(2):112-116.
DOI: 10.3872/j.issn.1007-385X.2017.02.002
Abstract:
Objective:To analyze the biological activity and plasma stability of specific aptamar W14 to metastatic colorectal cancer LoVo cell. Methods: Fluorescence microscopy was used to observe the specific binding activity of W14 to target LoVo cells under 25 ℃ and 37 ℃; Flow cytometry was used to detect W14 recognition ability of LoVo cell in plasma environment. W14 was respectively incubated in complete culture medium and human plasma for 0.5, 1, 1.5, 2, 3, 4 and 6 h under 37 ℃, and Agarose gel electrophoresis was used to observe the biological stability of aptamer W14; LoVo cells were treated with W14 at different concentrations (2，4，8，10 μmol/L) for 24, 48 and 72 h, and MTS was used to investigate the cytotoxicity of aptamer W14. Results: The aptamer W14 could specifically recognize the target LoVo cells under different temperatures and plasma environments, and it could stably exist in plasma for 6 hours without degradation, in addition, it had no obvious toxic effect on cells. Conclusion: Metastatic colorectal cancer-specific aptamer W14 is suitable for in vivo use, with superior adaptability, good biological stability and low toxicity.
Objective:To analyze the biological activity and plasma stability of specific aptamar W14 to metastatic colorectal cancer LoVo cell. Methods: Fluorescence microscopy was used to observe the specific binding activity of W14 to target LoVo cells under 25 ℃ and 37 ℃; Flow cytometry was used to detect W14 recognition ability of LoVo cell in plasma environment. W14 was respectively incubated in complete culture medium and human plasma for 0.5, 1, 1.5, 2, 3, 4 and 6 h under 37 ℃, and Agarose gel electrophoresis was used to observe the biological stability of aptamer W14; LoVo cells were treated with W14 at different concentrations (2，4，8，10 μmol/L) for 24, 48 and 72 h, and MTS was used to investigate the cytotoxicity of aptamer W14. Results: The aptamer W14 could specifically recognize the target LoVo cells under different temperatures and plasma environments, and it could stably exist in plasma for 6 hours without degradation, in addition, it had no obvious toxic effect on cells. Conclusion: Metastatic colorectal cancer-specific aptamer W14 is suitable for in vivo use, with superior adaptability, good biological stability and low toxicity.
2017, 24(2):117-121.
DOI: 10.3872/j.issn.1007-385X.2017.02.003
Abstract:
Objective:To establish a method for amplification ex vivo of natural killer (NK) cells derived from human umbilical cord blood and to investigate cytokilling effect of the NK cell on multiple cell lines of human esophageal cancer and primary generation tumor cells of the patients with esophageal cancer. Methods: Human cord blood mononuclear cells (CBMC) were isolated and, irradiated inactivation human leukemia K562 cell and IL-2, IL-15, IL-18 cytokines were added into to amplify NK cells in culture ex vivo for 2 weeks. Amplification results of the NK cells and killing ability of secreted cytolines IFN-γ and so on against the target K562 cell were detected by Flow cytometry assay. Effect of NK cell amplificated ex vivo from human umbilical cord blood on apoptosis of various esophageal cancer cell lines and primary generation cancer cell of the patients with esophageal cancer were examined. Results: Irradiated inactivation K562 cell combined with multiple cytokines can effectively amplified NK cell derived from human umbilical cord blood. After culture ex vivo for 2 weeks, percentage of the NK cell can reach about 80% and had obviously promoting apoptosis of the K562 cell. In addition, amplification ex vivo NK cell derived from human umbilical cord blood can promote apoptosis of the 6 cell lines of human esophageal cancer and the primary generation cancer cell of the patients with esophageal cancer. Conclusion: In the study, the method of amplification ex vivo of NK cells derived from human umbilical cord blood was successfully established. The promoting apoptosis effect of the NK cells on esophageal cancer cells might be confirmed. It could provide a novel approach for immunotherapy of esophageal cancer.
Objective:To establish a method for amplification ex vivo of natural killer (NK) cells derived from human umbilical cord blood and to investigate cytokilling effect of the NK cell on multiple cell lines of human esophageal cancer and primary generation tumor cells of the patients with esophageal cancer. Methods: Human cord blood mononuclear cells (CBMC) were isolated and, irradiated inactivation human leukemia K562 cell and IL-2, IL-15, IL-18 cytokines were added into to amplify NK cells in culture ex vivo for 2 weeks. Amplification results of the NK cells and killing ability of secreted cytolines IFN-γ and so on against the target K562 cell were detected by Flow cytometry assay. Effect of NK cell amplificated ex vivo from human umbilical cord blood on apoptosis of various esophageal cancer cell lines and primary generation cancer cell of the patients with esophageal cancer were examined. Results: Irradiated inactivation K562 cell combined with multiple cytokines can effectively amplified NK cell derived from human umbilical cord blood. After culture ex vivo for 2 weeks, percentage of the NK cell can reach about 80% and had obviously promoting apoptosis of the K562 cell. In addition, amplification ex vivo NK cell derived from human umbilical cord blood can promote apoptosis of the 6 cell lines of human esophageal cancer and the primary generation cancer cell of the patients with esophageal cancer. Conclusion: In the study, the method of amplification ex vivo of NK cells derived from human umbilical cord blood was successfully established. The promoting apoptosis effect of the NK cells on esophageal cancer cells might be confirmed. It could provide a novel approach for immunotherapy of esophageal cancer.
2017, 24(2):122-126.
DOI: 10.3872/j.issn.1007-385X.2017.02.004
Abstract:
Objective:To study effect of bridging intergrator 1(Bin 1) gene over-expression on cell cycle of non-small cell lung cancer H1975 line cell, and its mechanism. Methods: CMV-MCS-GFP-SV40-Neomucin-Bin1 plasmid carrying Bin1 gene was constructed and was transfected into the H1975 line cell (Bin1+ group). The H1975 line cell (Bin1- group) transfected with empty plasmid and the H1975 line cell (Control group) were set up. Expressions of Bin1 mRNA and protein in the H1975 cell of the 3 groups were respectively detected by RT-PCR and Western blotting assays. Cell cycle changes of the H1975 cell in the various treatment groups were examined by flow cytometry assay. Phosphorylation level of AKT and mTOR as well as expression of cell cycle related proteins (cyclinD1, CDK4 and Rb) in the various treatment groups were detected by Western blotting. Results: Comparing with the Bin1- and control groups, expressions of Bin1 mRNA and protein in the Bin1+ group were obviously up-regulation (P<0.05) , cell cycle of the H1975 cell in the Bin1+ group was blocked in G1 phase (\[60.53±1.89\]% vs \[46.14±1.56\]% and \[47.33±2.07\]%, P<005), and in the H1975 cell of the Bin1+ group, expressions of p-AKT and p-mTOR were significantly down-regulation (P<0.05) , expressions of AKT and mTOR were not significantly difference (P>0.05) , expressions of cyclinD1 and CDK4 proteins were markedly down-regulation and expression of Rb protein was evidently increased (P<0.05). Conclusion: Over-expression of Bin1 gene in the H195 cell could obviously induce blocking of the cell cycle and its mechanism might be caused by inhibiting AKT-mTOR pathway and its cell cycle related proteins.
Objective:To study effect of bridging intergrator 1(Bin 1) gene over-expression on cell cycle of non-small cell lung cancer H1975 line cell, and its mechanism. Methods: CMV-MCS-GFP-SV40-Neomucin-Bin1 plasmid carrying Bin1 gene was constructed and was transfected into the H1975 line cell (Bin1+ group). The H1975 line cell (Bin1- group) transfected with empty plasmid and the H1975 line cell (Control group) were set up. Expressions of Bin1 mRNA and protein in the H1975 cell of the 3 groups were respectively detected by RT-PCR and Western blotting assays. Cell cycle changes of the H1975 cell in the various treatment groups were examined by flow cytometry assay. Phosphorylation level of AKT and mTOR as well as expression of cell cycle related proteins (cyclinD1, CDK4 and Rb) in the various treatment groups were detected by Western blotting. Results: Comparing with the Bin1- and control groups, expressions of Bin1 mRNA and protein in the Bin1+ group were obviously up-regulation (P<0.05) , cell cycle of the H1975 cell in the Bin1+ group was blocked in G1 phase (\[60.53±1.89\]% vs \[46.14±1.56\]% and \[47.33±2.07\]%, P<005), and in the H1975 cell of the Bin1+ group, expressions of p-AKT and p-mTOR were significantly down-regulation (P<0.05) , expressions of AKT and mTOR were not significantly difference (P>0.05) , expressions of cyclinD1 and CDK4 proteins were markedly down-regulation and expression of Rb protein was evidently increased (P<0.05). Conclusion: Over-expression of Bin1 gene in the H195 cell could obviously induce blocking of the cell cycle and its mechanism might be caused by inhibiting AKT-mTOR pathway and its cell cycle related proteins.
2017, 24(2):127-133.
DOI: 10.3872/j.issn.1007-385X.2017.02.005
Abstract:
Objective:To prepare C-phycocyanin (C-PC) contained polymeric nanaparticles with targeting ligand and study its target treatment effect on HeLa cells. Methods: The targeting drug-loading carboxymethyl chitosan (CMC) nanoparticles were synthesized by ionic-gelation method, and the particles with the most optimal condition were selected by orthogonal analysis. The surface morphology and particles size were observed by transmission electron microscopy (TEM) and dynamic light scattering (DLS). The effects of nanoparticles on the proliferation of HeLa cells were assessed by MTT assay. The tissue compatibility and safety of nanoparticles were studied by hemolysis assay. The expression of cleaved Caspase-3 and Bcl-2 was determined by Western blotting and immunofluorescent staining, respectively. Results: The optimal condition for the preparation of the nanoparticles was: CMC at 2.0 mg/ml, CaCl2 at 1.0 mg/ml, and the nanoparticles size of about 120 nm with spherical morphology; the entrapment efficiency was (62±5)%; the ratio of CMC:C-PC was 3∶1, and drug-loading amount was (20±3)%. The drug-loading nanoparticles showed slow release characteristic in vitro and without hemolysis. The nanoparticles significantly inhibited the proliferation of HeLa cells and induced the cell apoptosis; in addition, it promoted the expressions of cleaved Caspase-3 protein but suppressed the expression of Bcl-2 protein. Conclusion: The novel targeting CPC nanoparticles could inhibit HeLa cell growth, with a superior apoptosis inducing effect over the other drugs, which provided a new idea for the research on marine drugs and an important theoretical value for further study on targeting drug-loading nanoparticles.
Objective:To prepare C-phycocyanin (C-PC) contained polymeric nanaparticles with targeting ligand and study its target treatment effect on HeLa cells. Methods: The targeting drug-loading carboxymethyl chitosan (CMC) nanoparticles were synthesized by ionic-gelation method, and the particles with the most optimal condition were selected by orthogonal analysis. The surface morphology and particles size were observed by transmission electron microscopy (TEM) and dynamic light scattering (DLS). The effects of nanoparticles on the proliferation of HeLa cells were assessed by MTT assay. The tissue compatibility and safety of nanoparticles were studied by hemolysis assay. The expression of cleaved Caspase-3 and Bcl-2 was determined by Western blotting and immunofluorescent staining, respectively. Results: The optimal condition for the preparation of the nanoparticles was: CMC at 2.0 mg/ml, CaCl2 at 1.0 mg/ml, and the nanoparticles size of about 120 nm with spherical morphology; the entrapment efficiency was (62±5)%; the ratio of CMC:C-PC was 3∶1, and drug-loading amount was (20±3)%. The drug-loading nanoparticles showed slow release characteristic in vitro and without hemolysis. The nanoparticles significantly inhibited the proliferation of HeLa cells and induced the cell apoptosis; in addition, it promoted the expressions of cleaved Caspase-3 protein but suppressed the expression of Bcl-2 protein. Conclusion: The novel targeting CPC nanoparticles could inhibit HeLa cell growth, with a superior apoptosis inducing effect over the other drugs, which provided a new idea for the research on marine drugs and an important theoretical value for further study on targeting drug-loading nanoparticles.
2017, 24(2):134-138.
DOI: 10.3872/j.issn.1007-385X.2017.02.006
Abstract:
Objective: To explore the immunological enhancement effect of dendritic cells (DCs) derived from peripheral blood mononuclear cells (PBMCs) pulsed CD40L+ lung cancer cell antigen , on homologous lung cancer. Methods: PBMCs were isolated from peripheral blood of adults by conventional methods, then induced differentiation into DCs; recombinant CD40L+A549 cell antigen was used for DC maturation stimulation. The expressions of CD83,CD86 and HLA-DR in DCs were detected by Flow Cytometry, IL-12 secretion was detected by ELISA; the effects of CD40L+ lung cancer cell antigen pulsed DCs on proliferation of homologous lymphocyte as well as A549 cells were examined by MTT, in addition, this effect was compared to the effect of DCs that pulsed by empty vector plasmid transfected A549 cell antigen. Results: Mature DCs were successfully induced from PBMCs. The expressions of CD83, CD86 and HLA-DR in CD40L+ A549-pulsed DC group were significantly higher than those in empty group (\[4.78±1.5\]% vs \[338±1.5\]%,\[9.79±5.27\]% vs \[5.53±2.17\]% and \[11.84±8.31\]% vs \[5.37±5.48\]%，all P<0.05\]; and the secretion of IL-12 in CD40L+ A549-pulsed DC group was also higher than those in empty group and untransfected group (P<0.05). In the mean while, CD40L-pulsed DCs significantly promoted the proliferation of lymphocytes (P<0.05), and its activated homologous T cells had a significantly higher inhibitory effect on A549 cell proliferation (P<0.05). Conclusion: DC pulsed by the tumor antigens from the reconstitution CD40L transfected A549 cells could enhance its specific immunity capacity against homologous lung cancer cells.
Objective: To explore the immunological enhancement effect of dendritic cells (DCs) derived from peripheral blood mononuclear cells (PBMCs) pulsed CD40L+ lung cancer cell antigen , on homologous lung cancer. Methods: PBMCs were isolated from peripheral blood of adults by conventional methods, then induced differentiation into DCs; recombinant CD40L+A549 cell antigen was used for DC maturation stimulation. The expressions of CD83,CD86 and HLA-DR in DCs were detected by Flow Cytometry, IL-12 secretion was detected by ELISA; the effects of CD40L+ lung cancer cell antigen pulsed DCs on proliferation of homologous lymphocyte as well as A549 cells were examined by MTT, in addition, this effect was compared to the effect of DCs that pulsed by empty vector plasmid transfected A549 cell antigen. Results: Mature DCs were successfully induced from PBMCs. The expressions of CD83, CD86 and HLA-DR in CD40L+ A549-pulsed DC group were significantly higher than those in empty group (\[4.78±1.5\]% vs \[338±1.5\]%,\[9.79±5.27\]% vs \[5.53±2.17\]% and \[11.84±8.31\]% vs \[5.37±5.48\]%，all P<0.05\]; and the secretion of IL-12 in CD40L+ A549-pulsed DC group was also higher than those in empty group and untransfected group (P<0.05). In the mean while, CD40L-pulsed DCs significantly promoted the proliferation of lymphocytes (P<0.05), and its activated homologous T cells had a significantly higher inhibitory effect on A549 cell proliferation (P<0.05). Conclusion: DC pulsed by the tumor antigens from the reconstitution CD40L transfected A549 cells could enhance its specific immunity capacity against homologous lung cancer cells.
2017, 24(2):139-144.
DOI: 10.3872/j.issn.1007-385X.2017.02.007
Abstract:
Objective:To investigate the expression of miRNA-93 and its effect on the cellular biological characteristics of bladder cancer cell line T24, and to explore the underlying mechanism.Methods:The cancer tissues and paired adjacent normal tissues from 79 patients with bladder cancer treated in Nanyang Center Hospital Affiliated to Zhengzhou University between May 2010 and May 2016 were selected for this study. The expressions of miRNA-93 were detected by Real-time PCR. After silencing of miRNA-93, the cell proliferation, apoptosis and migration were measured by CCK-8 assay, Flow cytometry and Transwell assay, respectively. The protein expressions of AKT/p-AKT and GSK3β/p-GSK3β were measured by Western blotting assay. Results: MiRNA-93 was highly expressed in both bladder cancer tissues and cancer cells (P<0.05), and its expression level was closely related to tumor size, lymph node metastasis, pathological grade stage and TNM classification (P<0.05). CCK-8 assay and cell cycle analysis showed that knockdown of miRNA-93 significantly suppressed T24 cell proliferation (P<0.05), and Flow Cytometry AnnexinV / PI double staining showed miRNA-93 silencing promoted T24 cell apoptosis (P<0.05). And Transwell assay showed that knockdown of miRNA-93 suppressed T24 cell migration. Furthermore, Western blotting showed that the protein expressions of p-AKT and p-GSK3β were significantly decreased after down-regulation of miRNA-93 (P<0.05). Conclusion:miRNA-93 could enhance cell proliferation and migration, and suppress cell apoptosis of human bladder cancer T24 cell line. And its mechanism might be related to the down-regulation of p-AKT and p-GSK3β protein expression, suggesting that miRNA-93 could be used as a potential new target for diagnostic and targeted therapy of bladder cancer.
Objective:To investigate the expression of miRNA-93 and its effect on the cellular biological characteristics of bladder cancer cell line T24, and to explore the underlying mechanism.Methods:The cancer tissues and paired adjacent normal tissues from 79 patients with bladder cancer treated in Nanyang Center Hospital Affiliated to Zhengzhou University between May 2010 and May 2016 were selected for this study. The expressions of miRNA-93 were detected by Real-time PCR. After silencing of miRNA-93, the cell proliferation, apoptosis and migration were measured by CCK-8 assay, Flow cytometry and Transwell assay, respectively. The protein expressions of AKT/p-AKT and GSK3β/p-GSK3β were measured by Western blotting assay. Results: MiRNA-93 was highly expressed in both bladder cancer tissues and cancer cells (P<0.05), and its expression level was closely related to tumor size, lymph node metastasis, pathological grade stage and TNM classification (P<0.05). CCK-8 assay and cell cycle analysis showed that knockdown of miRNA-93 significantly suppressed T24 cell proliferation (P<0.05), and Flow Cytometry AnnexinV / PI double staining showed miRNA-93 silencing promoted T24 cell apoptosis (P<0.05). And Transwell assay showed that knockdown of miRNA-93 suppressed T24 cell migration. Furthermore, Western blotting showed that the protein expressions of p-AKT and p-GSK3β were significantly decreased after down-regulation of miRNA-93 (P<0.05). Conclusion:miRNA-93 could enhance cell proliferation and migration, and suppress cell apoptosis of human bladder cancer T24 cell line. And its mechanism might be related to the down-regulation of p-AKT and p-GSK3β protein expression, suggesting that miRNA-93 could be used as a potential new target for diagnostic and targeted therapy of bladder cancer.
2017, 24(2):145-150.
DOI: 10.3872/j.issn.1007-385X.2017.02.008
Abstract:
Objective: To study the inhibitory effects of p-hydroxylcinnamaldehyde（CMSP）on the proliferation of esophageal cancer cells and the growth of their xenograft tumors on BABL/c nude mouse. Methods:The inhibitory effects of CMSP on the proliferation of Kyse 30 and TE-13 esophageal cancer cells were measured by cytometry. CEA and SCC mRNA expressions in esophageal cancer cells were detected with RT-PCR assay; the expression levels of C-myc and N-myc in esophageal cancer cells were detected by Western blotting; Esophageal cancer xenograft model was constructed on nude mouse, and the mice were divided into CMSP group and control group. After experiment ended, the tumor weight and size were measured. The expression levels of C-myc and N-myc in xenografts were detected by immunohistochemical SP assay; Morphological changes of liver, spleen and tumor tissues of nude mouse were observed by H-E staining under light microscope.Results: CMSP had obvious inhibitory effect on esophageal cancer cells Kyse 30 and TE-13（\[1.7±03\] vs \[3.8±0.3\]，\[1.6±0.2\] vs \[4.5±0.4\]，P<0.01）. Compared to the control group, after CMSP treatment,(1)the expressions of CEA and SCC mRNA in Kyse 30 and TE-13 cells were inhibited (P<0.01); the expressions of C-myc and N-myc proteins were significantly inhibited (P<0.05,P<0.01); (2) the average volume and weight of xenograft tumor in CMSP group significantly decreased (P<0.05,P<001); the expressions of C-myc and N-myc proteins were decreased. No obvious morphological changes were found in liver and spleen tissues in both CMSP treatment group and control group. Conclusion: CMSP has inhibitory effects on both esophageal cancer cells in vitro and their nude mouse xenograft tumors in vivo.
Objective: To study the inhibitory effects of p-hydroxylcinnamaldehyde（CMSP）on the proliferation of esophageal cancer cells and the growth of their xenograft tumors on BABL/c nude mouse. Methods:The inhibitory effects of CMSP on the proliferation of Kyse 30 and TE-13 esophageal cancer cells were measured by cytometry. CEA and SCC mRNA expressions in esophageal cancer cells were detected with RT-PCR assay; the expression levels of C-myc and N-myc in esophageal cancer cells were detected by Western blotting; Esophageal cancer xenograft model was constructed on nude mouse, and the mice were divided into CMSP group and control group. After experiment ended, the tumor weight and size were measured. The expression levels of C-myc and N-myc in xenografts were detected by immunohistochemical SP assay; Morphological changes of liver, spleen and tumor tissues of nude mouse were observed by H-E staining under light microscope.Results: CMSP had obvious inhibitory effect on esophageal cancer cells Kyse 30 and TE-13（\[1.7±03\] vs \[3.8±0.3\]，\[1.6±0.2\] vs \[4.5±0.4\]，P<0.01）. Compared to the control group, after CMSP treatment,(1)the expressions of CEA and SCC mRNA in Kyse 30 and TE-13 cells were inhibited (P<0.01); the expressions of C-myc and N-myc proteins were significantly inhibited (P<0.05,P<0.01); (2) the average volume and weight of xenograft tumor in CMSP group significantly decreased (P<0.05,P<001); the expressions of C-myc and N-myc proteins were decreased. No obvious morphological changes were found in liver and spleen tissues in both CMSP treatment group and control group. Conclusion: CMSP has inhibitory effects on both esophageal cancer cells in vitro and their nude mouse xenograft tumors in vivo.
2017, 24(2):151-157.
DOI: 10.3872/j.issn.1007-385X.2017.02.009
Abstract:
Objective:To observe the clinical efficacy of MASCTTM (multiple antigen stimulating cellular therapy) combined with transcatheter arterial chemoembolization (TACE) on primary hepatocellular carcinoma (HCC). Methods：The clinical data of 66 HCC patients with TACE during August 2010 to March 2015 in the Department of Infectious Diseases (Center of Liver Disease) of Nanfang Hospital were retrospectively analyzed. The patients were divided into combination group (TACE+ MASCTTM treatment) (32 patients) and TACE group (34 patients). The progression-free survival (PFS) and overall survival (OS) were evaluated in the two groups as main outcome measures. Results:The six-month, 1-year, 2-year PFS rates were 68.8%, 37.5%, 25% in combination group and 50%, 11.8%, 2.9% in TACE group, respectively. The median PFS was 9.5 months in combination group compared with 5.5 months in TACE group（P＜0.01）. The six-month, 1-year, 2-year OS rates were 81.3%, 65.6%, 40.6% in combination group and 91.2%, 47.1%, 23.5% in TACE group, respectively. The median OS was 19.5 months in combination group compared with 10.5 months in TACE group (P<0.05). MASCTTM, portal vein invasion, pretreatment serum AFP level and ECOG performance status were the independent prognostic factors for PFS, while MASCTTM, portal vein invasion and pretreatment serum TBIL level were the independent prognostic factors for OS. Conclusion: MASCTTM combined with TACE could robustly improve the clinical efficacy, and obviously prolong the PFS and OS for HCC patients.
Objective:To observe the clinical efficacy of MASCTTM (multiple antigen stimulating cellular therapy) combined with transcatheter arterial chemoembolization (TACE) on primary hepatocellular carcinoma (HCC). Methods：The clinical data of 66 HCC patients with TACE during August 2010 to March 2015 in the Department of Infectious Diseases (Center of Liver Disease) of Nanfang Hospital were retrospectively analyzed. The patients were divided into combination group (TACE+ MASCTTM treatment) (32 patients) and TACE group (34 patients). The progression-free survival (PFS) and overall survival (OS) were evaluated in the two groups as main outcome measures. Results:The six-month, 1-year, 2-year PFS rates were 68.8%, 37.5%, 25% in combination group and 50%, 11.8%, 2.9% in TACE group, respectively. The median PFS was 9.5 months in combination group compared with 5.5 months in TACE group（P＜0.01）. The six-month, 1-year, 2-year OS rates were 81.3%, 65.6%, 40.6% in combination group and 91.2%, 47.1%, 23.5% in TACE group, respectively. The median OS was 19.5 months in combination group compared with 10.5 months in TACE group (P<0.05). MASCTTM, portal vein invasion, pretreatment serum AFP level and ECOG performance status were the independent prognostic factors for PFS, while MASCTTM, portal vein invasion and pretreatment serum TBIL level were the independent prognostic factors for OS. Conclusion: MASCTTM combined with TACE could robustly improve the clinical efficacy, and obviously prolong the PFS and OS for HCC patients.
2017, 24(2):158-167.
DOI: 10.3872/j.issn.1007-385X.2017.02.010
Abstract:
Objective:To explore expressions of CDCA8 and INCENP mRNAs in hepatocellular carcinoma (HCC) and their clinical significance. Methods:Illumina Nextbio microarray database was used to analyze expressions of CDCA8 and INCENP mRNAs in primary HCC and paired adjacent liver tissues. The results were verified by the RNA-Seq mRNA expression data in liver cancer database of The Cancer Genome Atlas (TCGA). Then correlations of the CDCA8 and INCENPmRNAs expressions with clinicopathological features and prognosis of the patients with HCC were analyzed combining with clinical data of TCGA. Gene sets enrichment analysis (GSEA) software was used to analyze the related pathways for high expressions of the target genes. Results: The expression levels of CDCA8 and INCENP mRNAs were significantly upregulated in HCC tissues (P<0.01). The expression level of CDCA8 mRNA was significantly correlated with histological grade, clinical stage, tumor diameter, recurrence, Eastern Cooperative Oncology Group of the United States (ECOG) grade, serum alpha fetal protein (AFP) concentration and copy number alteration (CNA) of the patients with HCC (P<0.05). The expression level of INCENP mRNA was evidently correlated with histological grade, recurrence, ECOG grade, serum AFP concentration, mutation counts and CNA of the patients with HCC (P<0.05). Overall survival (OS) and tumor free survival (TFS) of the patients with higher expression level of CDCA8 mRNA were significantly shorter than those of the patients with lower expression level of CDCA8 mRNA (P<0.01). OS of the patients with higher expression level of INCENP mRNA was significantly shorter than that of the patients with lower expression level of INCENT mRNA (P<0.05). However, there was no significant difference of TFS between the patients with higher expression level and lower expression level of INCENT mRNA. Multivariate analysis showed that the expression level of CDCA8 mRNA was an independent factor for poor prognosis of the patients with HCC (P<0.01). Analization of GSEA indicated that CDCA8 and INCENT may play cerntain roles in other biological pathways except cell cycle-related pathways. Conclusion: Expressions of CDCA8 and INCENP mRNAs appeared significant high levels in HCC tissues. CDCA8could be as an independent risk factor for prognosis of HCC and a potential novel target for therapy of the patients with HCC.
Objective:To explore expressions of CDCA8 and INCENP mRNAs in hepatocellular carcinoma (HCC) and their clinical significance. Methods:Illumina Nextbio microarray database was used to analyze expressions of CDCA8 and INCENP mRNAs in primary HCC and paired adjacent liver tissues. The results were verified by the RNA-Seq mRNA expression data in liver cancer database of The Cancer Genome Atlas (TCGA). Then correlations of the CDCA8 and INCENPmRNAs expressions with clinicopathological features and prognosis of the patients with HCC were analyzed combining with clinical data of TCGA. Gene sets enrichment analysis (GSEA) software was used to analyze the related pathways for high expressions of the target genes. Results: The expression levels of CDCA8 and INCENP mRNAs were significantly upregulated in HCC tissues (P<0.01). The expression level of CDCA8 mRNA was significantly correlated with histological grade, clinical stage, tumor diameter, recurrence, Eastern Cooperative Oncology Group of the United States (ECOG) grade, serum alpha fetal protein (AFP) concentration and copy number alteration (CNA) of the patients with HCC (P<0.05). The expression level of INCENP mRNA was evidently correlated with histological grade, recurrence, ECOG grade, serum AFP concentration, mutation counts and CNA of the patients with HCC (P<0.05). Overall survival (OS) and tumor free survival (TFS) of the patients with higher expression level of CDCA8 mRNA were significantly shorter than those of the patients with lower expression level of CDCA8 mRNA (P<0.01). OS of the patients with higher expression level of INCENP mRNA was significantly shorter than that of the patients with lower expression level of INCENT mRNA (P<0.05). However, there was no significant difference of TFS between the patients with higher expression level and lower expression level of INCENT mRNA. Multivariate analysis showed that the expression level of CDCA8 mRNA was an independent factor for poor prognosis of the patients with HCC (P<0.01). Analization of GSEA indicated that CDCA8 and INCENT may play cerntain roles in other biological pathways except cell cycle-related pathways. Conclusion: Expressions of CDCA8 and INCENP mRNAs appeared significant high levels in HCC tissues. CDCA8could be as an independent risk factor for prognosis of HCC and a potential novel target for therapy of the patients with HCC.
2017, 24(2):168-173.
DOI: 10.3872/j.issn.1007-385X.2017.02.011
Abstract:
Objective:To explore Bcl-3 protein expression in human colorectal cancer and the effects of Bcl-3 gene silencing on proliferation and apoptosis of colorectal cancer HCT 116 cell line. Methods: 86 colorectal cancer tissues and the corresponding adjacent tissues from patients treated in Kunshan Hospital Affiliated to Jiangsu University between January 2012 and December 2015 were collected to analyze the correlation between Bcl-3 expression and clinicopathological features of colorectal cancer. Immunohistochemistry was used to detect Bcl-3 protein expression in 86 samples. HCT 116 cells were cultivated and divided into three groups: blank control group, control siRNA group (transfecting with control siRNA) and Bcl-3 siRNA (transfecting with Bcl-3 siRNA); and then Western blotting was used to determine Bcl-3 expression to verify the transfection efficiency. In addition, MTT, plate clone formation assay, Flow cytometry and streaming apoptosis assay were used to detect the proliferation, cloning formation, cell cycle distribution and the rate of apoptosis in each group, respectively. Results: IHC showed the positive expression rate of Bcl-3 protein in cancer tissues and adjacent normal tissues was 72.09% and 48.84% (P<0.05), respectively. The Bcl-3 protein expression in colorectal cancer tissues was positively correlated with histological grade, lymph node metastasis and Dukes staging (P<0.05). After being transfected for 48 h, the relative Bcl-3 expression level of blank control group and control siRNA group was significantly higher than that of Bcl-3 siRNA group (P<0.05), indicating successful transfection. MTT assay showed the absorbance value in all groups increased in a time-dependent manner. The optical density of Bcl-3 siRNA group was significantly lower than that of blank control group and control siRNA group at 24, 48, 72 and 96 h after transfection (P<0.05), and colony formation rate of Bcl-3 siRNA group was obviously lower than the other two groups (P<0.05). Flow cytomety showed that the proportion of G2 phase cells and cell apoptosis rate of Bcl-3 siRNA group was higher than those of blank control group and the control siRNA group (P<0.05). Conclusions: Bcl-3 protein expression in colorectal cancer tissues was positively correlated with histological grade, lymph node metastasis and Dukes staging; Bcl-3silencing might induce HCT 116 cell cycle arrest at G phase, suppress cell proliferation and colony formation, and promote cell apoptosis.
Objective:To explore Bcl-3 protein expression in human colorectal cancer and the effects of Bcl-3 gene silencing on proliferation and apoptosis of colorectal cancer HCT 116 cell line. Methods: 86 colorectal cancer tissues and the corresponding adjacent tissues from patients treated in Kunshan Hospital Affiliated to Jiangsu University between January 2012 and December 2015 were collected to analyze the correlation between Bcl-3 expression and clinicopathological features of colorectal cancer. Immunohistochemistry was used to detect Bcl-3 protein expression in 86 samples. HCT 116 cells were cultivated and divided into three groups: blank control group, control siRNA group (transfecting with control siRNA) and Bcl-3 siRNA (transfecting with Bcl-3 siRNA); and then Western blotting was used to determine Bcl-3 expression to verify the transfection efficiency. In addition, MTT, plate clone formation assay, Flow cytometry and streaming apoptosis assay were used to detect the proliferation, cloning formation, cell cycle distribution and the rate of apoptosis in each group, respectively. Results: IHC showed the positive expression rate of Bcl-3 protein in cancer tissues and adjacent normal tissues was 72.09% and 48.84% (P<0.05), respectively. The Bcl-3 protein expression in colorectal cancer tissues was positively correlated with histological grade, lymph node metastasis and Dukes staging (P<0.05). After being transfected for 48 h, the relative Bcl-3 expression level of blank control group and control siRNA group was significantly higher than that of Bcl-3 siRNA group (P<0.05), indicating successful transfection. MTT assay showed the absorbance value in all groups increased in a time-dependent manner. The optical density of Bcl-3 siRNA group was significantly lower than that of blank control group and control siRNA group at 24, 48, 72 and 96 h after transfection (P<0.05), and colony formation rate of Bcl-3 siRNA group was obviously lower than the other two groups (P<0.05). Flow cytomety showed that the proportion of G2 phase cells and cell apoptosis rate of Bcl-3 siRNA group was higher than those of blank control group and the control siRNA group (P<0.05). Conclusions: Bcl-3 protein expression in colorectal cancer tissues was positively correlated with histological grade, lymph node metastasis and Dukes staging; Bcl-3silencing might induce HCT 116 cell cycle arrest at G phase, suppress cell proliferation and colony formation, and promote cell apoptosis.
12 Analysis of clinical efficacy and prognosis of DC-CIK cellular immunotherapy in with gastric cancer
GAO Zuowen
,
ZHENG Jie
,
LOU Jinshu
,
SONG Desheng
,
YAO Lu
,
DING Tailiang
,
YANG Aizhen
,
JIANG Longwei
,
JIA Shaochang
2017, 24(2):174-179.
DOI: 10.3872/j.issn.1007-385X.2017.02.012
Abstract:
Objective:To retrospectively analyze safety and clinical efficacy of dendritic cells (DCs) combined with cytokine-induced killer (CIK) cellular immunotherapy in treatment of the 96 patients with gastric cancer (GC). Methods: Peripheral blood mononuclear cells (PBMCs) from the 96 GC patients who were hospitalized in the Oncology Department of the 86th Hospital of PLA and Tumor Biotherapy Center of the 81st Hospital of PLA during August 2011 to April 2016 were collected and cultured ex vivo to obtain DC and CIK cells. After sensitization with gastric cancer MGC-803 line cell lysates, the DCs combined with CIK cells were transfused back to the GC patients. Clinical efficacy and safety of the DC-CIK cellular immunotherapy were observed. Results: Overall response rate and disease control rate of the 96 GC patients following the DC-CIK immunotherapy were 15.6% and 55.2% respectively. Their 1 year survival rate was 56.0%, whereas rate of overall survival for 36-56 months was maintained at about 37.0%. No significant difference was observed in peripheral blood value of tumor markers, CEA, CA199 and CA724 of the GC patients between pretherapy and postherapy. After the DC-CIK immunotherapy the percentage of CD4+CD25+ Treg cell in peripheral blood of the GC patients was significantly decreased (\[3.22±1.20\]% vs \[2.46±1.04\]%, P<0.01), but the percentages of CD3+, CD4+, CD8+ and CD3+CD56+ T cell subsets as well as ratio of CD4+/CD8+ did not show any significant changes (P>0.05). Kaplan-Meier univariate analysis showed that TEM staging, times of the cellular immunotherapy as well as pretherapy value of CEA and CA199 were influence factors for prognosis of the GC patients treated with the DC-CIK cellular immunotherapy. Multivariate analysis with Cox model further indicated that times of the cellular immunotherapy as well as pretherapy value of CEA and CA199 were significantly associated with prognosis of the GC patients treated with the DC-CIK cellular immunotherapy (P<0.05). Conclusion: Autologous DC-CIK immunotherapy might be a safe and efficacy therapy approach for the GC patients, however multiple therapy of the DC-CIK immunotherapy could improve long-term survival rate of the patients with GC.
Objective:To retrospectively analyze safety and clinical efficacy of dendritic cells (DCs) combined with cytokine-induced killer (CIK) cellular immunotherapy in treatment of the 96 patients with gastric cancer (GC). Methods: Peripheral blood mononuclear cells (PBMCs) from the 96 GC patients who were hospitalized in the Oncology Department of the 86th Hospital of PLA and Tumor Biotherapy Center of the 81st Hospital of PLA during August 2011 to April 2016 were collected and cultured ex vivo to obtain DC and CIK cells. After sensitization with gastric cancer MGC-803 line cell lysates, the DCs combined with CIK cells were transfused back to the GC patients. Clinical efficacy and safety of the DC-CIK cellular immunotherapy were observed. Results: Overall response rate and disease control rate of the 96 GC patients following the DC-CIK immunotherapy were 15.6% and 55.2% respectively. Their 1 year survival rate was 56.0%, whereas rate of overall survival for 36-56 months was maintained at about 37.0%. No significant difference was observed in peripheral blood value of tumor markers, CEA, CA199 and CA724 of the GC patients between pretherapy and postherapy. After the DC-CIK immunotherapy the percentage of CD4+CD25+ Treg cell in peripheral blood of the GC patients was significantly decreased (\[3.22±1.20\]% vs \[2.46±1.04\]%, P<0.01), but the percentages of CD3+, CD4+, CD8+ and CD3+CD56+ T cell subsets as well as ratio of CD4+/CD8+ did not show any significant changes (P>0.05). Kaplan-Meier univariate analysis showed that TEM staging, times of the cellular immunotherapy as well as pretherapy value of CEA and CA199 were influence factors for prognosis of the GC patients treated with the DC-CIK cellular immunotherapy. Multivariate analysis with Cox model further indicated that times of the cellular immunotherapy as well as pretherapy value of CEA and CA199 were significantly associated with prognosis of the GC patients treated with the DC-CIK cellular immunotherapy (P<0.05). Conclusion: Autologous DC-CIK immunotherapy might be a safe and efficacy therapy approach for the GC patients, however multiple therapy of the DC-CIK immunotherapy could improve long-term survival rate of the patients with GC.
2017, 24(2):180-182.
DOI: 10.3872/j.issn.1007-385X.2017.02.013
Abstract:
目的：探讨苦参注射液对肺癌Lewis细胞的增殖、细胞周期、凋亡的影响。方法：采用MTT法及流式细胞技术，观察在不同浓度的苦参注射液处理24、48 h后，Lewis细胞增殖及细胞周期及凋亡的变化。结果: 肺癌Lewis细胞在苦参注射液作用下表现出增殖抑制，且呈现剂量、时间依赖趋势；经处理后的肺癌Lewis细胞周期阻滞于G1期；在苦参注射液促进Lewis细胞凋亡。结论:苦参注射液能有效将肺癌Lewis细胞周期阻滞在G0/G1期，使其细胞增殖率显著降低，同时提高其细胞凋亡率。
目的：探讨苦参注射液对肺癌Lewis细胞的增殖、细胞周期、凋亡的影响。方法：采用MTT法及流式细胞技术，观察在不同浓度的苦参注射液处理24、48 h后，Lewis细胞增殖及细胞周期及凋亡的变化。结果: 肺癌Lewis细胞在苦参注射液作用下表现出增殖抑制，且呈现剂量、时间依赖趋势；经处理后的肺癌Lewis细胞周期阻滞于G1期；在苦参注射液促进Lewis细胞凋亡。结论:苦参注射液能有效将肺癌Lewis细胞周期阻滞在G0/G1期，使其细胞增殖率显著降低，同时提高其细胞凋亡率。
2017, 24(2):183-188.
DOI: 10.3872/j.issn.1007-385X.2017.02.014
Abstract:
T细胞能够识别肿瘤抗原并特异性杀伤癌变细胞，是杀伤肿瘤的主要执行细胞，也是临床上研究最多的肿瘤治疗性免疫细胞。嵌合抗原受体基因修饰T（chimeric antigen receptor gene-modified T，CAR-T）细胞治疗能够绕过抗原提呈和MHC的限制，已在B急性淋巴细胞白血病（B-acute lymphoblastic leukemia，B-ALL）治疗中取得显著效果。近年来，越来越多的研究结果表明，CAR-T细胞同样可以用于实体瘤的治疗，如黑色素瘤、神经胶质瘤、卵巢癌、前列腺癌、肝细胞癌及其他常见实体瘤（转移性乳腺癌、胰腺癌）等。本文将对近年来CAR-T细胞免疫疗法在实体瘤临床转化的研究进展作一综述，主要从免疫抑制肿瘤微环境、脱靶毒性与细胞因子释放综合征（cytokine release syndrome，CRS）、肿瘤的异质性三个方面阐述CAR- T细胞治疗实体瘤的瓶颈，并对未来的发展加以展望。
T细胞能够识别肿瘤抗原并特异性杀伤癌变细胞，是杀伤肿瘤的主要执行细胞，也是临床上研究最多的肿瘤治疗性免疫细胞。嵌合抗原受体基因修饰T（chimeric antigen receptor gene-modified T，CAR-T）细胞治疗能够绕过抗原提呈和MHC的限制，已在B急性淋巴细胞白血病（B-acute lymphoblastic leukemia，B-ALL）治疗中取得显著效果。近年来，越来越多的研究结果表明，CAR-T细胞同样可以用于实体瘤的治疗，如黑色素瘤、神经胶质瘤、卵巢癌、前列腺癌、肝细胞癌及其他常见实体瘤（转移性乳腺癌、胰腺癌）等。本文将对近年来CAR-T细胞免疫疗法在实体瘤临床转化的研究进展作一综述，主要从免疫抑制肿瘤微环境、脱靶毒性与细胞因子释放综合征（cytokine release syndrome，CRS）、肿瘤的异质性三个方面阐述CAR- T细胞治疗实体瘤的瓶颈，并对未来的发展加以展望。
15 Anti-tumor effect of traditional Chinese medicine on the immunologic intervention of T lymphocytes
2017, 24(2):189-193.
DOI: 10.3872/j.issn.1007-385X.2017.02.015
Abstract:
中药具有一定的抗肿瘤疗效，不仅能够缓解肿瘤患者症状从而改善生活质量，还能在一定程度上控制肿瘤大小并延长患者生存期。由于T淋巴细胞在肿瘤细胞所产生的免疫应答中起主要作用，因此探索中药对T细胞免疫干预的作用机制可以为肿瘤治疗提供新的思路与方法。目前大多数中药通过促进T细胞因子释放、诱导细胞凋亡、增加T细胞总数及T辅助细胞、促进γδT细胞增殖等途径达到抗肿瘤作用。由于T细胞可分为αβT细胞与γδT细胞两大类，本文综合归纳了常用中药及其单体对αβT细胞与γδT细胞进行干预的主要机制，并提出了未来研究的方向，为进一步研究提供参考。
中药具有一定的抗肿瘤疗效，不仅能够缓解肿瘤患者症状从而改善生活质量，还能在一定程度上控制肿瘤大小并延长患者生存期。由于T淋巴细胞在肿瘤细胞所产生的免疫应答中起主要作用，因此探索中药对T细胞免疫干预的作用机制可以为肿瘤治疗提供新的思路与方法。目前大多数中药通过促进T细胞因子释放、诱导细胞凋亡、增加T细胞总数及T辅助细胞、促进γδT细胞增殖等途径达到抗肿瘤作用。由于T细胞可分为αβT细胞与γδT细胞两大类，本文综合归纳了常用中药及其单体对αβT细胞与γδT细胞进行干预的主要机制，并提出了未来研究的方向，为进一步研究提供参考。
2017, 24(2):194-200.
DOI: 10.3872/j.issn.1007-385X.2017.02.016
Abstract:
CXCL8（又名IL-8）具有3种受体，CXCL8结合不同受体则产生不同的生物学效应。CXCL8与多种类型肿瘤的发生发展有关，其中与结直肠癌及其肝转移的关系尤为密切。CXCL8与其受体相互作用后通过诱导肠癌细胞发生上皮间质转化、抵抗失巢凋亡以及免疫抑制等机制，促进肠癌细胞侵袭、迁移、释放入血形成循环肿瘤细胞（circulating tumor cells，CTCs），甚至促进CTCs存活以及定向趋化，进而在肝内定植形成转移灶。CXCL8及其受体还可介导肿瘤细胞-免疫细胞之间的相互作用，负向调节机体免疫功能，避免肿瘤细胞或CTCs免疫杀伤。本文综述有关CXCL8及其受体在结直肠癌进展和肝转移过程中的作用及其机制。
CXCL8（又名IL-8）具有3种受体，CXCL8结合不同受体则产生不同的生物学效应。CXCL8与多种类型肿瘤的发生发展有关，其中与结直肠癌及其肝转移的关系尤为密切。CXCL8与其受体相互作用后通过诱导肠癌细胞发生上皮间质转化、抵抗失巢凋亡以及免疫抑制等机制，促进肠癌细胞侵袭、迁移、释放入血形成循环肿瘤细胞（circulating tumor cells，CTCs），甚至促进CTCs存活以及定向趋化，进而在肝内定植形成转移灶。CXCL8及其受体还可介导肿瘤细胞-免疫细胞之间的相互作用，负向调节机体免疫功能，避免肿瘤细胞或CTCs免疫杀伤。本文综述有关CXCL8及其受体在结直肠癌进展和肝转移过程中的作用及其机制。
2017, 24(2):201-205.
DOI: 10.3872/j.issn.1007-385X.2017.02.017
Abstract:
成纤维细胞生长因子受体5(fibroblast growth factor receptor 5, FGFR5)是FGFR5家族中的一个新型受体，是由胞外区、穿膜区及胞内区构成的穿膜受体。然而，与其他经典FGFRs不同，其胞内区缺乏信号转导所必须的酪氨酸激酶，这一特征决定了其生物学功能有别于其他FGFRs。FGFR5激活时可抑制细胞增殖，促进细胞黏附和融合，提示该蛋白是一个潜在的抑癌因子，其分子机制有待进一步研究阐明。研究表明，FGFR5在肿瘤及非肿瘤疾病的发生发展中扮演了独特的角色。
成纤维细胞生长因子受体5(fibroblast growth factor receptor 5, FGFR5)是FGFR5家族中的一个新型受体，是由胞外区、穿膜区及胞内区构成的穿膜受体。然而，与其他经典FGFRs不同，其胞内区缺乏信号转导所必须的酪氨酸激酶，这一特征决定了其生物学功能有别于其他FGFRs。FGFR5激活时可抑制细胞增殖，促进细胞黏附和融合，提示该蛋白是一个潜在的抑癌因子，其分子机制有待进一步研究阐明。研究表明，FGFR5在肿瘤及非肿瘤疾病的发生发展中扮演了独特的角色。
2017, 24(2):206-210.
DOI: 10.3872/j.issn.1007-385X.2017.02.018
Abstract:
Ezrin蛋白作为ERM(Ezrin,Radixin, Moesin)家族的重要成员，其主要作用是参与细胞膜信号转导，维持细胞形态、运动和黏附，重塑细胞骨架等，还起到连接细胞膜和细胞骨架的作用。Ezrin蛋白在肿瘤细胞中的异常表达会影响肿瘤细胞的浸润及转移活性，说明Ezrin蛋白与肿瘤的发生、转移与预后密切相关。伴随着消化系统恶性肿瘤发病率的不断升高，严重影响到了人类的生活质量，探究Ezrin蛋白在肿瘤中的表达及其作用机制对于消化系统恶性肿瘤（如食管癌、结直肠癌、胃癌、肝癌、胰腺癌和胆道肿瘤）的早期诊断、治疗及预后评价等方面具有重要意义，同时也可为寻找新的基因治疗靶点及诊断用生物标志物提供新的依据。
Ezrin蛋白作为ERM(Ezrin,Radixin, Moesin)家族的重要成员，其主要作用是参与细胞膜信号转导，维持细胞形态、运动和黏附，重塑细胞骨架等，还起到连接细胞膜和细胞骨架的作用。Ezrin蛋白在肿瘤细胞中的异常表达会影响肿瘤细胞的浸润及转移活性，说明Ezrin蛋白与肿瘤的发生、转移与预后密切相关。伴随着消化系统恶性肿瘤发病率的不断升高，严重影响到了人类的生活质量，探究Ezrin蛋白在肿瘤中的表达及其作用机制对于消化系统恶性肿瘤（如食管癌、结直肠癌、胃癌、肝癌、胰腺癌和胆道肿瘤）的早期诊断、治疗及预后评价等方面具有重要意义，同时也可为寻找新的基因治疗靶点及诊断用生物标志物提供新的依据。
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Supported by:Beijing E-Tiller Technology Development Co., Ltd.