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MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma

BACKGROUND: We investigated the functional roles of microRNA-125a-5p in regulating human prostate carcinoma. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was conducted to evaluate the gene expression levels of miR-125a-5p in eight prostate cancer cell lines and nin...

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Autores principales: Fu, Yi, Cao, Fuhua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4689268/
https://www.ncbi.nlm.nih.gov/pubmed/26719710
http://dx.doi.org/10.2147/OTT.S92314
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author Fu, Yi
Cao, Fuhua
author_facet Fu, Yi
Cao, Fuhua
author_sort Fu, Yi
collection PubMed
description BACKGROUND: We investigated the functional roles of microRNA-125a-5p in regulating human prostate carcinoma. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was conducted to evaluate the gene expression levels of miR-125a-5p in eight prostate cancer cell lines and nine biopsy specimens from patients with prostate cancer. miR-125a-5p was genetically knocked down in prostate cancer cell lines, DU145 and VCaP cells by lentiviral transduction. The effects of miR-125a-5p downregulation on prostate cancer cell proliferation and migration were evaluated by MTT assay and transwell assay, respectively. Direct regulation of miR-125a-5p on its downstream targets, NAIF1, and apoptotic gene caspase-3 were evaluated through dual-luciferase reporter assay, qRT-PCR, and Western blot, respectively. NAIF1 was then ectopically overexpressed in DU145 and VCaP cells to modulate prostate cancer cell proliferation and migration. Finally, the effects of miR-125a-5p downregulation or NAIF1 overexpression on the growth of in vivo prostate cancer xenograft were evaluated. RESULTS: miR-125a-5p was upregulated in prostate cancer cell lines and human prostate carcinomas. Lentivirus induced miR-125a-5p downregulation in DU145 and VCaP cells inhibited prostate cancer cell proliferation or migration. NAIF1 was the direct target of miR-125a-5p, as both gene and protein expression levels of NAIF1, as well as caspase-3 were upregulated by miR-125a-5p. Forced overexpression of NAIF1 had similar antitumor effects as miR-125a-5p downregulation on prostate cancer cell proliferation and migration. In vivo prostate xenograft assay confirmed the tumor-suppressive effect of miR-125a-5p downregulation or NAIF1 overexpression. CONCLUSION: miR-125a-5p regulates prostate cancer cell proliferation and migration through NAIF1.
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spelling pubmed-46892682015-12-30 MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma Fu, Yi Cao, Fuhua Onco Targets Ther Original Research BACKGROUND: We investigated the functional roles of microRNA-125a-5p in regulating human prostate carcinoma. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was conducted to evaluate the gene expression levels of miR-125a-5p in eight prostate cancer cell lines and nine biopsy specimens from patients with prostate cancer. miR-125a-5p was genetically knocked down in prostate cancer cell lines, DU145 and VCaP cells by lentiviral transduction. The effects of miR-125a-5p downregulation on prostate cancer cell proliferation and migration were evaluated by MTT assay and transwell assay, respectively. Direct regulation of miR-125a-5p on its downstream targets, NAIF1, and apoptotic gene caspase-3 were evaluated through dual-luciferase reporter assay, qRT-PCR, and Western blot, respectively. NAIF1 was then ectopically overexpressed in DU145 and VCaP cells to modulate prostate cancer cell proliferation and migration. Finally, the effects of miR-125a-5p downregulation or NAIF1 overexpression on the growth of in vivo prostate cancer xenograft were evaluated. RESULTS: miR-125a-5p was upregulated in prostate cancer cell lines and human prostate carcinomas. Lentivirus induced miR-125a-5p downregulation in DU145 and VCaP cells inhibited prostate cancer cell proliferation or migration. NAIF1 was the direct target of miR-125a-5p, as both gene and protein expression levels of NAIF1, as well as caspase-3 were upregulated by miR-125a-5p. Forced overexpression of NAIF1 had similar antitumor effects as miR-125a-5p downregulation on prostate cancer cell proliferation and migration. In vivo prostate xenograft assay confirmed the tumor-suppressive effect of miR-125a-5p downregulation or NAIF1 overexpression. CONCLUSION: miR-125a-5p regulates prostate cancer cell proliferation and migration through NAIF1. Dove Medical Press 2015-12-17 /pmc/articles/PMC4689268/ /pubmed/26719710 http://dx.doi.org/10.2147/OTT.S92314 Text en © 2015 Fu and Cao. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Fu, Yi
Cao, Fuhua
MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma
title MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma
title_full MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma
title_fullStr MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma
title_full_unstemmed MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma
title_short MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma
title_sort microrna-125a-5p regulates cancer cell proliferation and migration through naif1 in prostate carcinoma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4689268/
https://www.ncbi.nlm.nih.gov/pubmed/26719710
http://dx.doi.org/10.2147/OTT.S92314
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