Open Access

ARTICLE

miR-365 Suppresses Cholangiocarcinoma Cell Proliferation and Induces Apoptosis by Targeting E2F2

Lunjian Chen^*, Xiaorong Huang^†, Xinxin Chen^‡

* Department of Hepatobiliary Surgery, The Xinjiang Uygur Autonomous Region People’s Hospital, Urumqi, P.R. China
† Otorhinolaryngology Center, The Xinjiang Uygur Autonomous Region People’s Hospital, Urumqi, P.R. China
‡ Department of Preventive Health Care, First Affiliated Hospital of Medical College of Shihezi University, Shihezi, P.R. China

Oncology Research 2018, 26(9), 1375-1382. https://doi.org/10.3727/096504018X15188352857437

Abstract

Cholangiocarcinoma (CCA) is one of the most malignant adenocarcinomas arising from bile duct epithelial cells. However, the molecular mechanism regulating CCA development and progression still needs to be investigated. Here we found that miR-365 was downregulated in CCA tissues compared with adjacent normal tissues. By functional experiments, we found that overexpression of miR-365 significantly inhibited CCA cell proliferation and promoted cellular apoptosis in vitro. Furthermore, administration with miR-365 markedly suppressed the growth of tumor tissues in vivo. Mechanistically, we identified E2F2 as the target gene of miR- 365 in CCA cells. We found that overexpression significantly inhibited the expression of E2F2 in CCA cells, and there was an inverse correlation between the expression levels of E2F2 and miR-365 in CCA tissues. We also found that E2F2 was highly expressed in CCA tissues and cell lines. Restoration of E2F2 in miR-365- overexpressing CCA cells promoted cell viability and reduced cellular apoptosis in CCA. Collectively, our study demonstrated the essential role of miR-365 and its functional mechanism in CCA cells, which provided a new insight on the design of therapeutic targets for CCA treatment.

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