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UHRF1 is regulated by miR‐124‐3p and promotes cell proliferation in intrahepatic cholangiocarcinoma
Author(s) -
Zhu Mengxuan,
Wei Chuanyuan,
Lin Jiajia,
Dong Shuangshuang,
Gao Dongmei,
Chen Jie,
Zhao Yan,
Liu Binbin
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28586
Subject(s) - cell growth , cancer research , cell cycle , in vivo , biology , in vitro , cell , proliferating cell nuclear antigen , g1 phase , intrahepatic cholangiocarcinoma , microrna , cell cycle checkpoint , microbiology and biotechnology , medicine , gene , genetics
Ubiquitin‐like with PHD and ring finger domains 1 (UHRF1) is abnormally overexpressed in multiple cancers and closely correlated with tumor‐promoting effects, such as high proliferation. However, how UHRF1 functions in intrahepatic cholangiocarcinoma (ICC) has not yet been determined. Herein, we found that UHRF1 is overexpressed in ICC tissues. Downregulated UHRF1 attenuated the transition of the G1/S cell cycle and then suppressed cell proliferation in vitro and tumor growth in vivo. Moreover, upstream regulators of the UHRF1 expression were predicted, and we found that direct binding of miR‐124‐3p inhibited the UHRF1 expression. Elevated miR‐124‐3p suppressed proliferation and led to the arrest of the cell cycle. Furthermore, the expression of UHRF1 was positively correlated with PCNA. Clinically, we showed that elevated UHRF1 was associated with poor prognosis, and served as an independent prognostic factor in ICC patients. Together, these findings demonstrate that UHRF1, regulated by miR‐124‐3p, acts as a tumor promoter by promoting cell proliferation in ICC.