MiRNA-1469 promotes lung cancer cells apoptosis through targeting STAT5a

MicroRNAs play key roles in cell growth, differentiation, and apoptosis. In this study, we described the regulation and function of miR-1469 in apoptosis of lung cancer cells (A549 and NCI-H1650). Expression analysis verified that miR-1469 expression significantly increased in apoptotic cells. Overe...

Full description

Saved in:
Bibliographic Details
Published inAmerican journal of cancer research Vol. 5; no. 3; pp. 1180 - 1189
Main Authors Xu, Chengshan, Zhang, Ling, Li, Hengheng, Liu, Zhihua, Duan, Lianning, Lu, Chengrong
Format Journal Article
LanguageEnglish
Published United States e-Century Publishing Corporation 01.01.2015
Subjects
Original
lung cancer
apoptosis
Stat5a
MicroRNA
Online AccessGet full text

Cover

More Information
Summary:MicroRNAs play key roles in cell growth, differentiation, and apoptosis. In this study, we described the regulation and function of miR-1469 in apoptosis of lung cancer cells (A549 and NCI-H1650). Expression analysis verified that miR-1469 expression significantly increased in apoptotic cells. Overexpression of miR-1469 in lung cancer cells increased cell apoptosis induced by etoposide. Additionally, we identified that Stat5a is a downstream target of miR-1469, which can bind directly to the 3'-untranslated region of the Stat5a, subsequently reducing both the mRNA and protein levels of Stat5a. Finally, co-expression of miR-1469 and Stat5a in A549 and NCI-H1650 cells partially abrogated the effect of miR-1469 on cell apoptosis. Our results show that miR-1469 functions as an apoptosis enhancer to regulate lung cancer apoptosis through targeting Stat5a and may become a critical therapeutic target in lung cancer.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:2156-6976
2156-6976