Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/37341
Title: MiR-1180 promotes apoptotic resistance to human hepatocellular carcinoma via activation of NF-κB signaling pathway
Authors: Tan, Guosheng
Wu, Linwei
Tan, Jinfu
Zhang, Bing
Chi-shing Tai, William
Xiong, Shiqiu
Chen, Wei
Yang, Jianyong
Li, Heping
First Published: 1-Mar-2016
Publisher: Nature Publishing Group
Citation: Scientific Reports, 2016, 6, 22328
Abstract: Apoptosis resistance in human hepatocellular carcinoma (HCC) is a significant factor in carcinogenesis. Therefore, understanding the molecular mechanisms involved in apoptosis resistance is crucial for developing anticancer therapies. Importantly, small non-coding microRNAs (miRNAs) have been reported as key biomarkers for detecting tumour onset and progression. In the present study, we demonstrate that miR-1180 is upregulated in HCC. Ectopic expression of miR-1180 has an anti-apoptotic effect in HCC, while miR-1180 inhibition increases cell apoptosis, both in vitro and in vivo. Moreover, our results show that miR-1180 directly targets key inhibitors of the nuclear factor (NF)-κB signaling pathway (i.e., OTUD7B and TNIP2) and the pro-apoptotic Bcl-2 associated death promoter (BAD) protein by post-transcriptional downregulation. Therefore, the anti-apoptotic function of miR-1180 in HCC may occur through NF-κB pathway activation via downregulation of its negative regulators. In conclusion, our study reveals the critical role of miR-1180 during apoptosis resistance in HCC.
DOI Link: 10.1038/srep22328
eISSN: 2045-2322
Links: http://www.nature.com/articles/srep22328
http://hdl.handle.net/2381/37341
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © the authors. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Appears in Collections:Published Articles, Dept. of Biochemistry

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