| Literature DB >> 30353165 |
Cheng Wang1,2,3,4, Yayun Gu1,2,3, Erbao Zhang1,2,3, Kai Zhang1,2,3, Na Qin1,2,3, Juncheng Dai1,2,3, Meng Zhu1,2,3, Jia Liu1,2,3, Kaipeng Xie1,2,3, Yue Jiang1,2,3, Xuejiang Guo1, Mingxi Liu1, Guangfu Jin1,2,3, Hongxia Ma1,2,3, Tao Jiang1,2,3, Rong Yin5, Yankai Xia6, Li Liu7, Shouyu Wang6, Bin Shen1, Ran Huo1, Lin Xu5, Jiahao Sha1, Bin Qu8, Hongbing Shen9,10,11, Zhibin Hu12,13,14.
Abstract
Our previous work found cancer-testis (CT) genes as a new source of epi-driver candidates of cancer. LIN28B was a CT gene, but the "driver" ability and the activation mechanism in lung adenocarcinoma (LUAD) remain unclear. We observed that LIN28B expression was restricted in testis. It was re-activated in LUAD patients without known genomic alterations in oncogenes and was related to poorer survival. In vitro and In vivo experiments confirmed that the activation of LIN28B could promote the proliferation and metastasis of LUAD cells and can influence cell cycle, DNA damage repair, and genome instability. In addition to the known let-7-LIN28B regulation loop, our results further revealed a let-7-independent Cis-regulator of LIN28B: LIN28B-AS1. LIN28B-AS1 is a CT long non-coding RNA (CT-lncRNA). It altered the messenger RNA stability of LIN28B by directly interacting with another CT protein IGF2BP1 but not with LIN28B and constituted a novel regulation network. In sum, we identify that LIN28B is an "epi-driver" of LUAD and clarify a new lncRNA-activated mechanism of LIN28B, which provide new candidate targets for precise anticancer therapy in the future.Entities:
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Year: 2018 PMID： 30353165 DOI： 10.1038/s41388-018-0548-x
Source DB: PubMed Journal: Oncogene ISSN： 0950-9232 Impact factor: 9.867