MicroRNA-1915-3p prevents the apoptosis of lung cancer cells by downregulating DRG2 and PBX2
Micro (mi)RNAs are short non-coding RNA molecules, which post-transcriptionally regulate gene expression and exert key roles in cell growth, differentiation and apoptosis. In the present study, the mechanism and the function of miR-1915-3p in the apoptotic regulation of lung cancer cell lines (NCI-H...
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Published in | Molecular medicine reports Vol. 13; no. 1; pp. 505 - 512 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Greece
D.A. Spandidos
01.01.2016
Spandidos Publications Spandidos Publications UK Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Micro (mi)RNAs are short non-coding RNA molecules, which post-transcriptionally regulate gene expression and exert key roles in cell growth, differentiation and apoptosis. In the present study, the mechanism and the function of miR-1915-3p in the apoptotic regulation of lung cancer cell lines (NCI-H441 and NCI-H1650) were investigated. The expression analysis confirmed that the expression of miR-1915-3p was markedly decreased in the apoptotic cells. The overexpression of miR-1915-3p in the lung cancer cells prevented apoptosis induced by etoposide. Developmentally regulated GTP-binding protein 2 (DRG2) and pre-B cell leukemia homeobox 2 (PBX2) were identified as downstream targets of miR-1915-3p, which was shown to bind directly to the 3′-untranslated region of DRG2 and PBX2, subsequently lowering their mRNA and protein expression levels. Co-expression of miR-1915-3p and DRG2/PBX2 in the NCI-H441 and NCI-H1650 cells partly circumvented the effect of miR-1915-3p on apoptosis. The results in the present study revealed that miR-1915-3p functions as a silencer of apoptosis, which regulates lung cancer apoptosis via targeting DRG2/PBX2, and consequently this miRNA may be a putative therapeutic target in lung cancer. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1791-2997 1791-3004 |
DOI: | 10.3892/mmr.2015.4565 |