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Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13

BACKGROUND: This study aims to investigate the effects of inhibiting microRNA-9-5p (miR-9-5p) on the expression of StAR-related lipid transfer domain containing 13 (StarD13) and the progress of prostate cancer. METHODS: The mRNA expression levels of miR-9-5p and StarD13 were determined in several pr...

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Autores principales: Chen, Lin, Hu, Weifeng, Li, Guohao, Guo, Yonglian, Wan, Zhihua, Yu, Jiajun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6408831/
https://www.ncbi.nlm.nih.gov/pubmed/30899277
http://dx.doi.org/10.1186/s11658-019-0145-1
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author Chen, Lin
Hu, Weifeng
Li, Guohao
Guo, Yonglian
Wan, Zhihua
Yu, Jiajun
author_facet Chen, Lin
Hu, Weifeng
Li, Guohao
Guo, Yonglian
Wan, Zhihua
Yu, Jiajun
author_sort Chen, Lin
collection PubMed
description BACKGROUND: This study aims to investigate the effects of inhibiting microRNA-9-5p (miR-9-5p) on the expression of StAR-related lipid transfer domain containing 13 (StarD13) and the progress of prostate cancer. METHODS: The mRNA expression levels of miR-9-5p and StarD13 were determined in several prostate cancer cell lines. We chose DU145 and PC-3 cells for further research. The CCK8 assay was used to measure the cell viability. The cell invasion and wound-healing assays were respectively applied to evaluate invasion and migration. The expression of E-cadherin (E-cad), N-cadherin (N-cad) and vimentin were measured via western blot. DU145 and PC-3 cells overexpressing StarD13 were generated to investigate the variation in proliferation, invasion and migration. A luciferase reporter assay was used to identify the target of miR-9-5p. RESULTS: Our results show that miR-9-5p was highly expressed and StarD13 was suppressed in prostate cancer cells. MiR-9-5p inhibition repressed the cells’ viability, invasion and migration. It also increased the expression of E-cad and decreased that of N-cad and vimentin. StarD13 overexpression gave the same results as silencing of miR-9-5p: suppression of cell proliferation, invasion and migration. The bioinformatics analysis predicted StarD13 as a target gene of miR-9-5p. Quantitative RT-PCR, western blot analysis and the dual-luciferase reporter assay were employed to confirm the prediction. CONCLUSION: Our results show that miR-9-5p plays a powerful role in the growth, invasion, migration and epithelial–mesenchymal transition (EMT) of prostate cancer cells by regulating StarD13. A therapeutic agent inhibiting miR-9-5p could act as a tumor suppressor for prostate cancer.
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spelling pubmed-64088312019-03-21 Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13 Chen, Lin Hu, Weifeng Li, Guohao Guo, Yonglian Wan, Zhihua Yu, Jiajun Cell Mol Biol Lett Research BACKGROUND: This study aims to investigate the effects of inhibiting microRNA-9-5p (miR-9-5p) on the expression of StAR-related lipid transfer domain containing 13 (StarD13) and the progress of prostate cancer. METHODS: The mRNA expression levels of miR-9-5p and StarD13 were determined in several prostate cancer cell lines. We chose DU145 and PC-3 cells for further research. The CCK8 assay was used to measure the cell viability. The cell invasion and wound-healing assays were respectively applied to evaluate invasion and migration. The expression of E-cadherin (E-cad), N-cadherin (N-cad) and vimentin were measured via western blot. DU145 and PC-3 cells overexpressing StarD13 were generated to investigate the variation in proliferation, invasion and migration. A luciferase reporter assay was used to identify the target of miR-9-5p. RESULTS: Our results show that miR-9-5p was highly expressed and StarD13 was suppressed in prostate cancer cells. MiR-9-5p inhibition repressed the cells’ viability, invasion and migration. It also increased the expression of E-cad and decreased that of N-cad and vimentin. StarD13 overexpression gave the same results as silencing of miR-9-5p: suppression of cell proliferation, invasion and migration. The bioinformatics analysis predicted StarD13 as a target gene of miR-9-5p. Quantitative RT-PCR, western blot analysis and the dual-luciferase reporter assay were employed to confirm the prediction. CONCLUSION: Our results show that miR-9-5p plays a powerful role in the growth, invasion, migration and epithelial–mesenchymal transition (EMT) of prostate cancer cells by regulating StarD13. A therapeutic agent inhibiting miR-9-5p could act as a tumor suppressor for prostate cancer. BioMed Central 2019-03-08 /pmc/articles/PMC6408831/ /pubmed/30899277 http://dx.doi.org/10.1186/s11658-019-0145-1 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Chen, Lin
Hu, Weifeng
Li, Guohao
Guo, Yonglian
Wan, Zhihua
Yu, Jiajun
Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
title Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
title_full Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
title_fullStr Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
title_full_unstemmed Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
title_short Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
title_sort inhibition of mir-9-5p suppresses prostate cancer progress by targeting stard13
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6408831/
https://www.ncbi.nlm.nih.gov/pubmed/30899277
http://dx.doi.org/10.1186/s11658-019-0145-1
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