Chengdu Lilai Biotechnology Co., Ltd, Chengdu, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, West China Second University Hospital, SiChuan University, Chengdu, China.
Cell Biochem Funct. 2020 Jul;38(5):541-548. doi: 10.1002/cbf.3489. Epub 2020 Feb 13.
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). SIGNIFICANCE OF THE STUDY: These findings suggested that CLDN6 may act as an oncogene in HCC and improve HepG2 cell proliferation, migration, and invasion may via EGFR/AKT/mTOR signalling pathway.
越来越多的证据表明，claudin-6（CLDN6）在许多癌症中表达异常，而其在肝细胞癌（HCC）中的表达和生物学功能尚不清楚。本研究表明，CLDN6 在 HCC 组织中的表达高于肿瘤相邻组织。CLDN6 沉默显著抑制 HepG2 细胞的增殖、迁移和侵袭。同时，下调 CLDN6 显著抑制了 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。研究意义：这些发现表明，CLDN6 可能在 HCC 中作为癌基因发挥作用，通过 EGFR/AKT/mTOR 信号通路改善 HepG2 细胞的增殖、迁移和侵袭。
