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
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
复制标题
DOI：
10.1016/j.cellsig.2019.109462
复制
发表时间：
2020-02-01
影响因子：
4.8
通讯作者：
Wang, Enhua
中科院分区：
文献类型：
--
作者：
Liang, Yuan;Rong, Xuezhu;Wang, Enhua
肺腺癌是影响全球人群的非小细胞肺癌中最常见的亚型。近年来的研究表明，长链非编码rna （IncRNAs）具有调控基因表达的能力。最初，我们发现LINC00355在肺腺癌组织和细胞中的表达增加。功能上，我们的研究结果表明，LINC00355沉默可以抑制体外和体内的增殖。此外，我们发现LINC00355在肺腺癌细胞中负调控miR-195。同时，shRNA沉默LINC00355可通过miR-195抑制增殖、集落形成，促进细胞周期阻滞和凋亡。此外，shRNA沉默LINC00355可通过miR-195抑制肺腺癌细胞中细胞周期蛋白El （CCNE1）基因的表达。综上所述，本研究证实了新型lncRNA LINC00355在肺腺癌中通过miR-195参与CCNE1的调控网络，突出了LINC00355作为治疗肺腺癌的新靶点。
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 (IncRNAs) 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 El (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.