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Retracted : LncRNA ATB promotes proliferation and metastasis in A549 cells by down‐regulation of microRNA‐494
Author(s) -
Cao Yiwei,
Luo Xiangjun,
Ding Xiaoqian,
Cui Shichao,
Guo Caihong
Publication year - 2018
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.26894
Subject(s) - a549 cell , stat3 , protein kinase b , cancer research , cell growth , epithelial–mesenchymal transition , transfection , western blot , microrna , cell migration , biology , microbiology and biotechnology , signal transduction , chemistry , cell , cell culture , metastasis , cancer , gene , biochemistry , genetics
Lung cancer is a commonly diagnosed disease with poor prognosis. Novel therapeutic targets and deep understanding of the regulatory mechanisms in lung cancer are of great importance. We aimed to figure out the functional roles of lncRNA‐activated by transforming growth factor‐β (ATB) in A549 cells as well as the underlying molecular mechanisms. ATB was non‐physiologically expressed in A549 cells after cell transfection. Then, cell proliferation, expressions of proteins related to proliferation and epithelial‐mesenchymal transition (EMT), migration, and invasion were measured by BrdU incorporation assay, Western blot analysis, and Transwell assay, respectively. Afterwards, miR‐494 expression in transfected A549 cells was determined by quantitative reverse transcription PCR. Meanwhile, effects of miR‐494 overexpression on ATB‐overexpressed cells were assessed. Finally, the phosphorylation levels of AKT and key kinases in the Janus‐activated kinase (JAK)/signal transducer and activator of transcription‐3 (STAT3) pathway were detected by Western blot analysis. ATB overexpression promoted proliferation, migration, and invasion of A549 cells. Meanwhile, EMT of A549 cells was also enhanced. ATB silence showed the opposite influence. Expression of miR‐494 was negatively regulated by ATB. Following experiments showed ATB‐induced alterations of proliferation, migration, invasion, and EMT were all reversed by miR‐494 overexpression. Finally, we proved that ATB increased phosphorylated levels of AKT, JAK1, and STAT3, and those increases were all reversed by miR‐494 overexpression. We interestingly figured out that ATB promoted proliferation, migration, invasion, and EMT through down‐regulating miR‐494 in A549 cells. Moreover, ATB might activate AKT and the JAK/STAT3 pathway via down‐regulating miR‐494.