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LncRNA‐PCAT‐1 promotes non–small cell lung cancer progression by regulating miR‐149‐5p/LRIG2 axis
Author(s) -
Li Jie,
Li Yingjie,
Wang Bin,
Ma Yongfu,
Chen Ping
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28046
Subject(s) - cancer research , gene knockdown , downregulation and upregulation , lung cancer , cell growth , biology , microrna , cell cycle , apoptosis , suppressor , cancer , gene , medicine , genetics
Long noncoding RNAs (lncRNAs) are key players in the development and progression of human cancers. The lncRNA PCAT‐1 has been shown to be upregulated in human non–small cell lung cancer (NSCLC); however, its role and molecular mechanisms in NSCLC cell progression remain unclear. Here, we found that the higher expression of PCAT‐1 led to a significantly poorer survival time, and multivariate analysis revealed that PCAT‐1 was an independent risk factor of prognosis in NSCLC. Furthermore, we also found that the knockdown of PCAT‐1 remarkably suppressed cell growth by inducing cell cycle arrest and apoptosis promotion in NSCLC cells. Moreover, the bioinformatics analysis and luciferase reporter assay revealed that PCAT‐1 directly bound to the miR‐149‐5p, which has been reported to act as a tumor suppressor in diverse cancers. In addition, our results confirmed that the tumor‐promoting effects of PCAT‐1 in NSCLC cells are at least partly through negative modulation of miR‐149‐5p. Finally, mechanistic investigations showed that PCAT‐1 upregulated the expression of miR‐149‐5p target gene leucine‐rich repeats and immunoglobulin (Ig)‐like domains 2 (LRIG2) through competitively “spongeing” miR‐149‐5p. Therefore, we concluded that PCAT‐1 may promote the development of NSCLC through the miR‐149‐5p/LRIG2 axis.