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miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway

The current study aimed to investigate the potential role of miR-9 in the inhibition of ovarian cancer progression through the stromal cell-derived factor-1 (SDF-1)/ C-X-C chemokine receptor type 4 (CXCR4) pathway and to provide a theoretical basis for the diagnosis and treatment of ovarian cancer....

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Autores principales: He, Lin, Zhang, Li, Wang, Mengfei, Wang, Wenrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377313/
https://www.ncbi.nlm.nih.gov/pubmed/28413458
http://dx.doi.org/10.3892/etm.2017.4118
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author He, Lin
Zhang, Li
Wang, Mengfei
Wang, Wenrong
author_facet He, Lin
Zhang, Li
Wang, Mengfei
Wang, Wenrong
author_sort He, Lin
collection PubMed
description The current study aimed to investigate the potential role of miR-9 in the inhibition of ovarian cancer progression through the stromal cell-derived factor-1 (SDF-1)/ C-X-C chemokine receptor type 4 (CXCR4) pathway and to provide a theoretical basis for the diagnosis and treatment of ovarian cancer. Human ovarian cancer OVCAR-3 cells were transfected with miR-9 short hairpin RNA (shRNA). The effect of miR-9 on the mRNA expression levels of CXCR4 were analyzed using reverse transcription-quantitative polymerase chain reaction. The effects of miR-9 on OVCAR-3 cell proliferation, invasion and apoptotic ability were detected using a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay, Matrigel method, and Annexin V-fluorescein isothiocyanate flow cytometry, respectively. In addition, expression levels of SDF-1/CXCR4 pathway associated proteins were determined by western blot analysis. mRNA expression levels of CXCR4 in OVCAR-3 cells transfected with miR-9 shRNA was significantly downregulated compared with the blank and control groups (P<0.05). Furthermore, compared with the two control groups, the current results revealed that miR-9 inhibited cell proliferation, suppressed invasive ability and induced cell apoptosis in OVCAR-3 cells (P<0.05). Finally, it was observed that miR-9 functioned as a tumor inhibitor through the SDF-1/CXCR4 pathway by suppressing the expression levels of extracellular signal-regulated kinase 1 (ERK1), ERK2 and matrix metalloproteinase-9 proteins. The present study suggested that miR-9 may function as a promising tumor inhibitor for ovarian cancer through targeting the SDF-1/CXCR4 pathway.
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spelling pubmed-53773132017-04-15 miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway He, Lin Zhang, Li Wang, Mengfei Wang, Wenrong Exp Ther Med Articles The current study aimed to investigate the potential role of miR-9 in the inhibition of ovarian cancer progression through the stromal cell-derived factor-1 (SDF-1)/ C-X-C chemokine receptor type 4 (CXCR4) pathway and to provide a theoretical basis for the diagnosis and treatment of ovarian cancer. Human ovarian cancer OVCAR-3 cells were transfected with miR-9 short hairpin RNA (shRNA). The effect of miR-9 on the mRNA expression levels of CXCR4 were analyzed using reverse transcription-quantitative polymerase chain reaction. The effects of miR-9 on OVCAR-3 cell proliferation, invasion and apoptotic ability were detected using a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay, Matrigel method, and Annexin V-fluorescein isothiocyanate flow cytometry, respectively. In addition, expression levels of SDF-1/CXCR4 pathway associated proteins were determined by western blot analysis. mRNA expression levels of CXCR4 in OVCAR-3 cells transfected with miR-9 shRNA was significantly downregulated compared with the blank and control groups (P<0.05). Furthermore, compared with the two control groups, the current results revealed that miR-9 inhibited cell proliferation, suppressed invasive ability and induced cell apoptosis in OVCAR-3 cells (P<0.05). Finally, it was observed that miR-9 functioned as a tumor inhibitor through the SDF-1/CXCR4 pathway by suppressing the expression levels of extracellular signal-regulated kinase 1 (ERK1), ERK2 and matrix metalloproteinase-9 proteins. The present study suggested that miR-9 may function as a promising tumor inhibitor for ovarian cancer through targeting the SDF-1/CXCR4 pathway. D.A. Spandidos 2017-04 2017-02-10 /pmc/articles/PMC5377313/ /pubmed/28413458 http://dx.doi.org/10.3892/etm.2017.4118 Text en Copyright: © He et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
He, Lin
Zhang, Li
Wang, Mengfei
Wang, Wenrong
miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway
title miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway
title_full miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway
title_fullStr miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway
title_full_unstemmed miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway
title_short miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway
title_sort mir-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the sdf-1/cxcr4 pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377313/
https://www.ncbi.nlm.nih.gov/pubmed/28413458
http://dx.doi.org/10.3892/etm.2017.4118
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