CLCA4 inhibits cell proliferation and invasion of hepatocellular carcinoma by suppressing epithelial-mesenchymal transition via PI3K/AKT signaling | Zendy

Zhao Liu | Zendy; Chen Mi | Zendy; Linka Xie | Zendy; Ting Liu | Zendy; Zhenwei Zou | Zendy; Yong Li | Zendy; Peng Chen | Zendy; Xin Peng | Zendy; Charlie Ma | Zendy; Wenjie Zhang | Zendy; Pindong Li | Zendy

Open Access

CLCA4 inhibits cell proliferation and invasion of hepatocellular carcinoma by suppressing epithelial-mesenchymal transition via PI3K/AKT signaling

Author(s) -

Zhao Liu,

Chen Mi,

Linka Xie,

Ting Liu,

Zhenwei Zou,

Yong Li,

Peng Chen,

Xin Peng,

Charlie Ma,

Wenjie Zhang,

Pindong Li

Publication year - 2018

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.101571

Subject(s) - epithelial–mesenchymal transition , pi3k/akt/mtor pathway , gene knockdown , protein kinase b , cancer research , hepatocellular carcinoma , immunohistochemistry , biology , cell growth , phosphorylation , cell migration , signal transduction , cell , pathology , medicine , metastasis , cell culture , cancer , microbiology and biotechnology , genetics

Calcium activated Chloride Channel A4 (CLCA4), as a tumor suppressor, was reported to contribute to the progression of several malignant tumors, yet little is known about the significance of CLCA4 in invasion and prognosis of hepatocellular carcinoma (HCC). CLCA4 expression was negatively correlated with tumor size, vascular invasion and TNM stage. Kaplan-Meier analysis showed that CLCA4 was an independent predictor for overall survival (OS) and time to recurrence (TTR). In addition, CLCA4 status could act as prognostic predictor in different risk of subgroups. Moreover, combination of CLCA4 and serum AFP could be a potential predictor for survival in HCC patients. Furthermore, CLCA4 may inhibit cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) via PI3K/ATK signaling. Knockdown of CLCA4 significantly increased the migration and invasion of HCC cells and changed the expression pattern of EMT markers and PI3K/AKT phosphorylation. An opposite expression pattern of EMT markers and PI3K/AKT phosphorylation was observed in CLCA4-transfected cells. Additionally, immunohistochemistry and RT-PCR results further confirmed this correlation. Taken together, CLCA4 contributes to migration and invasion by suppressing EMT via PI3K/ATK signaling and predicts favourable prognosis of HCC. CLCA4/AFP expression may help to distinguish different risks of HCC patients after hepatectomy.

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