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Authors He M, Xue Y
Received 29 September 2016
Accepted for publication 2 November 2016
Published 2 March 2017 Volume 2017:10 Pages 1353—1361
DOI https://doi.org/10.2147/OTT.S123518
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 2
Editor who approved publication: Dr Ingrid Espinoza
Abstract: Lung cancer has the highest morbidity and mortality in the world, and
non-small cell lung carcinomas (NSCLC) account for 80% of cases of lung cancer.
The mechanism of NSCLC is still largely unknown, and finding novel targets is
of great importance for the treatment of NSCLC. The current study was designed
to evaluate the role of miR-148a in NSCLC cell proliferation and invasion and
to investigate the possible molecular mechanisms. We found that miR-148a
expression was decreased in NSCLC tissues and cell lines. Upregulation of miR-148a
significantly decreased A549 cell proliferation, and downregulation of miR-148a
significantly increased A549 cell proliferation. Upregulation of miR-148a
markedly increased apoptotic cell death and inhibited cell invasion potential.
Upregulation of miR-148a significantly decreased signal transducer and
activator of transcription 3 (STAT3) expression and 3'-untranslated region
luciferase activity. Downregulation of miR-148a significantly increased STAT3
expression. Overexpression of STAT3 significantly inhibited the effect of
miR-148a on cell viability and invasion potential. In conclusion, we found that
miR-148a inhibited NSCLC cell proliferation and invasion potential through the
inhibition of STAT3. Our findings highlight miR-148a/STAT3 axis as a novel
therapeutic target for the inhibition of NSCLC growth.
Keywords: miR-148a, STAT3, non-small cell lung
carcinomas, cell proliferation, invasion