Accumulating evidence showed that the claudin‐6 (CLDN6) expression was abnormal in many cancers, while its expression and biological functions in hepatocellular carcinoma (HCC) is still unclear. The present study demonstrated that CLDN6 was upregulated in HCC tissues compared with tumour‐adjacent tissues. CLDN6 silencing was significantly inhibited proliferation, migration, and invasion of HepG2 cells. Meanwhile, downregulation of CLDN6 remarkably inhibited the activation of EGFR/AKT/mTOR signalling pathway. Interestingly, the effect of CLDN6 overexpression on HepG2 cell proliferation and invasion could be inhibited by EGFR/AKT/mTOR signalling pathway inhibitor (AG1478).

中文翻译：

---

CLDN6的下调通过调节肝细胞癌中的EGFR / AKT / mTOR信号传导途径抑制细胞增殖，迁移和侵袭。

越来越多的证据表明，claudin-6（CLDN6）的表达在许多癌症中都是异常的，而其在肝细胞癌（HCC）中的表达和生物学功能仍不清楚。本研究表明，与癌旁组织相比，CLDN6在肝癌组织中上调。CLDN6沉默显着抑制HepG2细胞的增殖，迁移和侵袭。同时，CLDN6的下调显着抑制了EGFR / AKT / mTOR信号通路的激活。有趣的是，EGFR / AKT / mTOR信号通路抑制剂（AG1478）可抑制CLDN6过表达对HepG2细胞增殖和侵袭的影响。