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LncRNA F11‐AS1 suppresses liver hepatocellular carcinoma progression by competitively binding with miR‐3146 to regulate PTEN expression
Author(s) -
Du Junkai,
Chen Mingyue,
Liu Jianfei,
Hu Pan,
Guan Hong,
Jiao Xiaoqin
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29163
Subject(s) - pten , hepatocellular carcinoma , cancer research , biology , microbiology and biotechnology , signal transduction , pi3k/akt/mtor pathway
Accumulating evidence has proved that long noncoding RNAs (lncRNAs) are involved in cancer progression. The abnormal expression of lncRNAs might mediate cancer in various ways. Liver hepatocellular carcinoma (LIHC) is the third leading cause of tumor‐related deaths. Due to the difficulty in its early recognition, the therapeutic outcomes of LIHC are far from satisfactory. The lncRNA Coagulation Factor XI Antisense RNA 1 (F11‐AS1) is underexpressed in LIHC and suppresses LIHC progression in return. F11‐AS1 can bind with and negatively regulate miR‐3146, while miR‐3146 can bind with and negatively regulate PTEN. Moreover, F11‐AS1 positively regulates the messenger RNA and protein level of PTEN. Also, miR‐3146, F11‐AS1, and PTEN could all be immunoprecipitated by antibody against Ago2, indicating the existence of RNA–induced silencing complex. Therefore, F11‐AS1 mediates PTEN expression by acting as competing endogenous RNA of miR‐3146. Further rescue assays demonstrated that F11‐AS1 suppressed LIHC progression via such pattern. To sum up, F11‐AS1 suppresses LIHC progression by competitively binding with miR‐3146 to regulate PTEN expression. The F11‐AS1/miR‐3146/PTEN axis is brand new. Taken together, the results indicate that F11‐AS1 might serve as a therapeutic target of LIHC.