| Literature DB >> 31689506 |
Yuan Liang1, Xuezhu Rong2, Yuan Luo2, Pengcheng Li2, Qiang Han2, Lai Wei2, Enhua Wang3.
Abstract
Lung adenocarcinoma is the most common subtype of non-small-cell lung cancer affecting people all over the globe. Recent studies have indicated that long non-coding RNAs (lncRNAs) possess the ability to regulate gene expression. Initially, we uncovered increased LINC00355 expressions in lung adenocarcinoma tissues and cells. Functionally, our findings demonstrated that LINC00355 silencing suppressed the proliferation in vitro and in vivo. In addition, we found that LINC00355 negatively regulated miR-195 in lung adenocarcinoma cells. Simultaneously, silencing LINC00355 by shRNA resulted in suppressed proliferation, colony formation and promoted cell cycle arrest and apoptosis via miR-195. Moreover, silencing LINC00355 by shRNA inhibited the cyclin E1 (CCNE1) gene expression via miR-195 in lung adenocarcinoma cells. Collectively, this study demonstrates the novel lncRNA LINC00355 in regulatory network of CCNE1 via miR-195 in lung adenocarcinoma, highlighting LINC00355 as a new target for the treatment of lung adenocarcinoma.Entities:
Keywords: CCNE1; LINC00355; Lung adenocarcinoma; MicroRNA-195; Proliferation
Year: 2019 PMID: 31689506 DOI: 10.1016/j.cellsig.2019.109462
Source DB: PubMed Journal: Cell Signal ISSN: 0898-6568 Impact factor: 4.315