LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling
Authors E C, Yang J, Li H, Li C
Received 12 December 2018
Accepted for publication 25 February 2019
Published 11 April 2019 Volume 2019:11 Pages 2871—2879
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Cristina Weinberg
Peer reviewer comments 3
Editor who approved publication: Dr Ahmet Emre Eskazan
Changyong E,1 Jinghui Yang,1 Hang Li,2 Chunsheng Li3
1Department of Hepatobiliary and Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, People’s Republic of China; 2Department of Cerebral Surgery, Jilin Cancer Hospital, Changchun 130000, People’s Republic of China; 3Department of Gastrointestinal Colorectal and Anal surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, People’s Republic of China
Background: Recently, a growing number of long noncoding RNAs (lncRNAs) have been identified to be important for human cancer development. However, how lncRNA regulates hepatocellular carcinoma (HCC) progression still remains largely unclear. We aimed to investigate the function of LOC105372579 in HCC progression.
Materials and methods: The expression levels of lncRNA LOC105372579 in HCC tissues and cell lines were analyzed by qRT-PCR. The effects of LOC105372579 silencing on proliferation, migration and invasion were determined by using cell counting kit-8, colony formation assay and Transwell assay. Moreover, the xenograft mouse model was used to detect how LOC105372579 regulates HCC growth in vivo.
Results: LOC105372579 was highly expressed in HCC tissues and cell lines. Moreover, upregulated levels of LOC105372579 predicted poor prognosis. LOC105372579 silencing suppressed the proliferation of HCC cells in vitro. We also validated that LOC105372579 knockdown inhibited the migration, invasion, and epithelial–mesenchymal transition of HCC cells. Xenograft assay demonstrated that LOC105372579 promotes tumor growth in vivo. Mechanistically, we identified that LOC105372579 is a sponge for miR-4316 and that FOXP4 is a direct target of miR-4316.
Conclusion: Thus, our findings supported that LOC105372579 contributes to HCC cell proliferation, migration, invasion, and EMT by activating miR-4316/FOXP4 signaling.
Keywords: LOC105372579, HCC, proliferation, EMT, progression
Corrigendum for this paper has been published.
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