A novel long non-coding RNA LINC00355 promotes proliferation of lung adenocarcinoma cells by down-regulating miR-195 and up-regulating the expression of CCNE1

Cell Signal. 2020 Feb:66:109462. doi: 10.1016/j.cellsig.2019.109462. Epub 2019 Nov 2.

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.

Keywords: CCNE1; LINC00355; Lung adenocarcinoma; MicroRNA-195; Proliferation.

MeSH terms

  • Adenocarcinoma of Lung / genetics
  • Adenocarcinoma of Lung / metabolism*
  • Animals
  • Apoptosis
  • Cell Cycle Checkpoints
  • Cell Line, Tumor
  • Cell Proliferation
  • Cyclin E / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Male
  • Mice
  • Mice, Nude
  • MicroRNAs / metabolism*
  • Oncogene Proteins / metabolism*
  • RNA, Long Noncoding / metabolism*

Substances

  • CAHM long non-coding RNA, human
  • CCNE1 protein, human
  • Cyclin E
  • MIRN195 microRNA, human
  • MicroRNAs
  • Oncogene Proteins
  • RNA, Long Noncoding