Language:

miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells

PloS one, 2013-03, Vol.8 (3), p.e60317-e60317 [Peer Reviewed Journal]

COPYRIGHT 2013 Public Library of Science ;2013 Chen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2013 Chen et al 2013 Chen et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0060317 ;PMID: 23555954

Full text available

Citations Cited by

Actions
1. Add to My Research
2. Remove from My Research
3. E-mail
4. Print
5. Permalink
6. Citation
7. EasyBib
8. EndNote
9. RefWorks
10. Delicious
11. Export RIS
12. Export BibTeX

Title:
miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells
Author: Chen, Gang ; Umelo, Ijeoma Adaku ; Lv, Shasha ; Teugels, Erik ; Fostier, Karel ; Kronenberger, Peter ; Dewaele, Alex ; Sadones, Jan ; Geers, Caroline ; De Grève, Jacques
Chellappan, Srikumar P.
Subjects: Adult ; Aged ; Aged, 80 and over ; Antibodies, Monoclonal, Humanized - pharmacology ; Antineoplastic Agents - pharmacology ; Apoptosis ; Biology ; Biomarkers ; Breast cancer ; Cancer ; Cancer therapies ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Carcinoma, Non-Small-Cell Lung/drug therapy/genetics/metabolism/pathology ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell proliferation ; Cell Proliferation - drug effects ; Cervical cancer ; Cetuximab ; Chemotherapy ; Cytokines ; Development and progression ; Drug delivery ; Epidermal growth factor receptors ; ErbB Receptors - metabolism ; Female ; Gefitinib ; Gene expression ; Gene Expression Regulation, Neoplastic ; Growth ; Health aspects ; Human health sciences ; Humans ; Inhibition ; Kinases ; Laboratories ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lung cancer ; Lung cancer, Non-small cell ; Lung cancer, Small cell ; Lung diseases ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Lung Neoplasms/drug therapy/genetics/metabolism/pathology ; Lung/drug effects/metabolism/pathology ; Male ; Medical prognosis ; Medicine ; Metastases ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; MicroRNAs/genetics/metabolism ; Middle Aged ; miRNA ; Monoclonal antibodies ; Mutation ; NF-kappa B - metabolism ; NF-κB protein ; Non-small cell lung carcinoma ; Oncologie ; Oncology ; Pancreatic cancer ; Paraffin ; Pathology ; Patients ; Phenotypes ; Receptor, Epidermal Growth Factor/metabolism ; Ribonucleic acid ; RNA ; Sciences de la santé humaine ; Sensitizing ; Signal Transduction ; Signaling ; siRNA ; Targeted cancer therapy ; Thyroid cancer ; Tumors
Is Part Of: PloS one, 2013-03, Vol.8 (3), p.e60317-e60317
Description: 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-κB 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<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<0.05). miR-146a is therefore a strong candidate prognostic biomarker in NSCLC. Thus inducing miR-146a might be a therapeutic strategy for NSCLC.
Publisher: United States: Public Library of Science
Language: English
Identifier: ISSN: 1932-6203
EISSN: 1932-6203
DOI: 10.1371/journal.pone.0060317
PMID: 23555954
Source: Open Access: DOAJ Directory of Open Access Journals
Freely Accessible Journals
PLoS (Open access)
AUTh Library subscriptions: ProQuest Central
MEDLINE
PubMed Central

Back to results list


INSPIRE LIBRARY - TON DUC THANG UNIVERSITY	(84-028) 37 755 057	Feedback
19 Nguyen Huu Tho St. Dist.7, HCM	thuvien@tdtu.edu.vn	Feedback

miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells

Searching Remote Databases, Please Wait