JAM-A通过调控FAK/ERK信号通路对宫颈癌细胞进展的影响  

Effect of JAM-A on cervical cancer cell progression by regulating FAK/ERK signaling pathway

作　　者：赵晨阳[1] 彭丽秀[1] 邓赫男[1] 谭琛[1] 张玮[1] 何昌晖 邓美林 李琼[1] ZHAO Chenyang;PENG Lixiu;DENG Henan;TAN Chen;ZHANG Wei;HE Changhui;DENG Meilin;LI Qiong(Chenzhou First People's Hospital,the First Affiliated Hospital of Xiangnan University,Chenzhou,Hunan 423000,China)

机构地区：[1]郴州市第一人民医院/湘南学院第一附属医院,湖南郴州423000

出　　处：《中国优生与遗传杂志》2023年第9期1760-1766,共7页Chinese Journal of Birth Health & Heredity

基　　金：湘南学院校级科研项目(2021XJ107)。

摘　　要：目的 探讨连接黏附分子A(JAM-A)在宫颈癌细胞进展中的作用及其潜在分子机制。方法 实时荧光定量PCR(RT-qPCR)实验检测JAM-A在宫颈癌患者癌组织中的表达水平。将Vector、pcDNA-JAM-A、NC-siRNA、JAM-A-siRNA质粒分别转染至宫颈癌细胞中,CCK-8检测细胞增殖能力;Transwell实验检测细胞侵袭能力;细胞划痕实验检测细胞迁移能力;Western blotting分别检测细胞中JAM-A、PCNA、MMP-2、E-cadherin及FAK/ERK通路蛋白的水平。进行裸鼠皮下成瘤实验,检测JAM-A对宫颈癌细胞体内肿瘤生长的影响。结果 与癌旁组织比较,宫颈癌组织中JAM-A mRNA和蛋白水平均显著上调。过表达JAM-A可显著增强细胞增殖、侵袭和迁移能力,升高JAM-A、PCNA、MMP-2蛋白表达,降低E-cadherin蛋白表达。敲低JAM-A可显著抑制细胞增殖、侵袭和迁移能力,降低JAM-A、PCNA、MMP-2蛋白表达,升高E-cadherin蛋白表达。pcDNA-JAM-A+PF-562271组细胞中p-ERK2蛋白表达较pcDNA-JAM-A+Vehicle组显著降低。pcDNA-JAM-A组裸鼠皮下肿瘤的质量和体积较Vector组显著增加。结论 过表达JAM-A通过调控FAK-ERK2信号通路促进宫颈癌细胞增殖、侵袭和迁移。Objective To investigate the role of junctional adhesion molecule A(JAM-A)in cervical cancer cell progression and its potential molecular mechanism.Methods Real-time quantitative PCR(RT-qPCR)assay was used to detect the expression level of JAM-A in cancer tissues of cervical cancer patients.Cervical cancer cells were transfected with Vector,pcDNA-JAM-A,NC-siRNA and JAM-A-siRNA plasmids,respectively.CCK-8 was used to detect cell proliferation ability.Transwell assay was used to detect cell invasion ability.Wound healing assay was used to detect cell migration ability.Western blotting was used to detect the levels of JAM-A,PCNA,MMP-2,E-cadherin and FAK/ERK pathway proteins in cells,respectively.The effect of JAM-A on tumor growth in cervical cancer cells was detected by subcutaneous tumor-forming experiment in nude mice.Results Compared with adjacent tissues,the mRNA and protein levels of JAM-A were significantly up-regulated in cervical cancer tissues.Overexpression of JAM-A significantly enhanced cell proliferation,invasion and migration,increased the protein expression of JAM-A,PCNA and MMP-2,and decreased the protein expression of E-cadherin.Knockdown of JAM-A significantly inhibited cell proliferation,invasion and migration,decreased the protein expression of JAM-A,PCNA and MMP-2,and increased the protein expression of E-cadherin.The expression of p-ERK2 protein in pcDNA-JAMA+PF-562271 group was significantly lower than that in pcDNA-JAM-A+Vehicle group.The weight and volume of subcutaneous tumors in the pcDNA-JAM-A group were significantly higher than those in the Vector group.Conclusion JAM-A overexpression promotes the proliferation,invasion and migration of cervical cancer cells by regulating the FAK-ERK2 signaling pathway.

关 键 词：连接黏附分子A 宫颈癌 侵袭 迁移 FAK/ERK信号通路 

分 类 号：R737.33[医药卫生—肿瘤]