miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells
Authors: Erik Teugels
Karel Fostier
Peter Kronenberger
Jan Sadones
Alex Dewaele
Gang Chen
Jacques De Gr√®ve
Ijeoma Adaku Umelo
Shasha Lv
Caroline Geers
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: microRNA-146a; non-small cell lung cancer; cell growth; apoptosis; EGFR signaling
Affiliations: Department of Pathology, First Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi, People's Republic of China.

Abstract:  Aberrant expression of microRNA-146a (miR-146a) has been reported to be involved in the development and progression of various types of cancers. However, its role in non-small cell lung cancer (NSCLC) has not been elucidated. The aim of this study was to investigate the contribution of miR-146a to various aspects of the malignant phenotype of human NSCLCs. In functional experiments, miR-146a suppressed cell growth, induced cellular apoptosis and inhibited EGFR downstream signaling in five NSCLC cell lines (H358, H1650, H1975, HCC827 and H292). miR-146a also inhibited the migratory capacity of these NSCLC cells. On the other hand, miR-146a enhanced the inhibition of cell proliferation by drugs targeting EGFR, including both TKIs (gefitinib, erlotinib, and afatinib) and a monoclonal antibody (cetuximab). These effects were independent of the EGFR mutation status (wild type, sensitizing mutation or resistance mutation), but were less potent compared to the effects of siRNA targeting of EGFR. Our results suggest that these effects of miR-146a are due to its targeting of EGFR and NF-Œ∫B signaling. We also found, in clinical formalin fixed paraffin embedded (FFPE) lung cancer samples, that low expression of miR-146a was correlated with advanced clinical TNM stages and distant metastasis in NSCLC (P&lt;0.05). The patients with high miR-146a expression in their tumors showed longer progression-free survival (25.6 weeks in miR-146a high patients vs. 4.8 weeks in miR-146a low patients, P&lt;0.05). miR-146a is therefore a strong candidate prognostic biomarker in NSCLC. Thus inducing miR-146a might be a therapeutic strategy for NSCLC. 

Retracted: No

PubPeer comments:
 Figure 8, bottom panels. * Shown with red boxes: the 0h Inhi panel looks very similar to the 0h Si panel. The lines drawn around the scratch are slightly different. Could the authors please check?  , 
 Chen G, et al. miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells. PLoS One. 2013;8(3):e60317. Dear Dr. Elisabeth M Bik: Thank you so much. Without your reminder, we might never realize this mistake. Indeed, the image of the 0h Si panel in H1975 cells was wrong, which probably occurred in the figure preparation. Here is the corrected figure:  We have submitted an erratum to the journal of PLOS ONE. We have also rechecked all the raw data and raw pictures of these wound healing experiments, and we can confirm that all of the figure legends, results and conclusions remain unchanged. As the first author of the paper, I take full responsibility for this error. I made this mistake before paper submission, and did not find it during the subsequent revision and proof review. I sincerely apologize for this mistake to all my co-authors, the journal of PLOS ONE, and all the readers. Thank you again for your excellent reminder. Best regards Gang Chen , 
 Thank you, Dr. Chen, for correcting this error. ,