CD44v6通过ERK途径促进子宫内膜癌的增殖和转移  

CD44v6 promote the proliferation and metastasis of endometrial cancer by ERK pathway

作　　者：龙佑梅 黄梨 王艳清[1] 夏良斌[1] LONG Youmei;HUANG Li;WANG Yanqing;XIA Liangbin(Department of Gynecology,People's Hospital of Wuhan University,Wuhan Hubei 430060,P.R.China)

机构地区：[1]武汉大学人民医院妇二科,湖北武汉430060

出　　处：《中国计划生育和妇产科》2020年第7期76-79,I0002,I0003,共6页Chinese Journal of Family Planning & Gynecotokology

摘　　要：目的探究CD44v6的表达水平是否与子宫内膜癌(endometrial carcinoma,EC)的进展有关,并探讨其分子途径和生物学过程。方法收集2017年1月至2018年12月在武汉大学人民医院妇产科接受分期手术的30例手术标本,包括EC及距离癌组织2 cm处的癌旁非肿瘤内膜组织,采用免疫组织化学染色法检测CD44v6、ERK和磷酸化ERK(p-ERK)在EC组织中的表达。采用实时定量聚合酶链反应检测CD44v6在EC组织和细胞系中的表达,蛋白质印迹法检测相关蛋白的表达,最后进行克隆、迁移和侵袭试验。结果 CD44v6和p-ERK在EC组织中的表达明显增强。Western blot及PCR结果显示si-CD44v6可明显抑制CD44v6的表达,当CD44v6的表达受到抑制后,p-ERK的蛋白水平也降低。细胞克隆、转移和侵袭实验结果显示,抑制CD44v6表达可以抑制Ishikawa细胞的克隆、增殖和侵袭能力,但是可以通过ERK激动剂来逆转这种效果。结论 CD44v6在EC组织中高表达,且能够通过促进ERK蛋白磷酸化,从而促进EC的侵袭和转移,导致EC患者不良的预后。推测阻断CD44v6与ERK通路的传导是治疗EC的潜在方法。Objective To investigate whether the expression level of CD44 v6 is related to the progress of endometrial carcinoma(EC),and to explore its molecular pathways and biological processes.Methods A total of 30 surgical specimens,including EC and non-tumor endometrial tissues adjacent to the cancer tissue 2 cm away from the cancer tissue,were collected from January 2017 to December 2018 in the staged surgery in Department of Obstetrics and Gynecology of People ’s Hospital of Wuhan University.Immunohistochemical staining was used to detect CD44 v6,ERK and phosphorylated ERK(p-ERK) expression in EC tissues.Realtime quantitative polymerase chain reaction was used to detect the expression of CD44 v6 in EC tissues and cell lines.Western blot was used to detect the expression of related proteins.Finally,cloning,transwell and invasion tests were performed.Results The expression of CD44 v6 and p-ERK in EC tissues was significantly enhanced.Western blot and PCR results showed that si-CD44 v6 can significantly inhibit the expression of CD44 v6.When the expression of CD44 v6 was suppressed,the protein level of p-ERK also decreased.The results of cell cloning,metastasis and invasion experiments showed that inhibition of CD44 v6 expression can inhibit the cloning,proliferation and invasion ability of Ishikawa cells,but this effect can be reversed by ERK agonists.Conclusion CD44 v6 is highly expressed in EC tissues,and it can promote the invasion and metastasis of EC by promoting ERK protein phosphorylation,leading to poor prognosis of EC patients.It is speculated that blocking the conduction of CD44 v6 and ERK pathway is a potential treatment for EC.

关 键 词：子宫内膜癌 粘附分子 CD44V6 P-ERK 

分 类 号：R737.33[医药卫生—肿瘤]