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miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1

Cutaneous squamous cell carcinoma (cSCC) accounts for 20% of non-melanoma skin cancer worldwide. MicroRNAs (miRNAs or miRs) are a subtype of non-coding RNA associated with the progression of various types of human cancer. MiR-186 has been demonstrated to act as an oncogene in human tumors. However,...

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Autores principales: Tian, Jing, Shen, Rui, Yan, Yuzhang, Deng, Liehua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6176155/
https://www.ncbi.nlm.nih.gov/pubmed/30344679
http://dx.doi.org/10.3892/etm.2018.6679
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author Tian, Jing
Shen, Rui
Yan, Yuzhang
Deng, Liehua
author_facet Tian, Jing
Shen, Rui
Yan, Yuzhang
Deng, Liehua
author_sort Tian, Jing
collection PubMed
description Cutaneous squamous cell carcinoma (cSCC) accounts for 20% of non-melanoma skin cancer worldwide. MicroRNAs (miRNAs or miRs) are a subtype of non-coding RNA associated with the progression of various types of human cancer. MiR-186 has been demonstrated to act as an oncogene in human tumors. However, the role of miR-186 in cSCC remains unclear. The expression of miR-186 and apoptotic protease activating factor 1 (APAF1) was examined using reverse transcription-quantitative polymerase chain reaction, western blotting and immunofluorescence. The correlation between miR-186 and APAF1 was determined using a dual-luciferase assay. Mimics or inhibitors of miR-186 were transfected into A-431 cells to establish cell lines with overexpressed or knocked-down miR-186, respectively. EdU staining and colony formation assays were performed to detect cell proliferation. Transwell and wound-healing assays were performed to analyze cell invasion and migration, respectively. Hoechst staining and flow cytometry were performed to assess cell apoptosis and cell cycle distribution. MiR-186 expression was significantly increased, while APAF1 expression was significantly decreased in cSCC tissues compared with the controls. An miR-186 binding site was predicted in APAF1 and their expression was negatively correlated in cSCC tissues. Cell proliferation, invasion and migration were significantly enhanced in the miR-186-overexpressed A-431 cells and attenuated in miR-186 knockdown cells compared with the control. APAF1 expression was regulated by miR-186, while APAF1 knockdown significantly promoted cell invasion and inhibited cell apoptosis. In summary, the results of the present study indicate that miR-186 serves as an oncogene in cSCC by inhibiting APAF1.
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spelling pubmed-61761552018-10-21 miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1 Tian, Jing Shen, Rui Yan, Yuzhang Deng, Liehua Exp Ther Med Articles Cutaneous squamous cell carcinoma (cSCC) accounts for 20% of non-melanoma skin cancer worldwide. MicroRNAs (miRNAs or miRs) are a subtype of non-coding RNA associated with the progression of various types of human cancer. MiR-186 has been demonstrated to act as an oncogene in human tumors. However, the role of miR-186 in cSCC remains unclear. The expression of miR-186 and apoptotic protease activating factor 1 (APAF1) was examined using reverse transcription-quantitative polymerase chain reaction, western blotting and immunofluorescence. The correlation between miR-186 and APAF1 was determined using a dual-luciferase assay. Mimics or inhibitors of miR-186 were transfected into A-431 cells to establish cell lines with overexpressed or knocked-down miR-186, respectively. EdU staining and colony formation assays were performed to detect cell proliferation. Transwell and wound-healing assays were performed to analyze cell invasion and migration, respectively. Hoechst staining and flow cytometry were performed to assess cell apoptosis and cell cycle distribution. MiR-186 expression was significantly increased, while APAF1 expression was significantly decreased in cSCC tissues compared with the controls. An miR-186 binding site was predicted in APAF1 and their expression was negatively correlated in cSCC tissues. Cell proliferation, invasion and migration were significantly enhanced in the miR-186-overexpressed A-431 cells and attenuated in miR-186 knockdown cells compared with the control. APAF1 expression was regulated by miR-186, while APAF1 knockdown significantly promoted cell invasion and inhibited cell apoptosis. In summary, the results of the present study indicate that miR-186 serves as an oncogene in cSCC by inhibiting APAF1. D.A. Spandidos 2018-11 2018-09-03 /pmc/articles/PMC6176155/ /pubmed/30344679 http://dx.doi.org/10.3892/etm.2018.6679 Text en Copyright: © Tian 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
Tian, Jing
Shen, Rui
Yan, Yuzhang
Deng, Liehua
miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
title miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
title_full miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
title_fullStr miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
title_full_unstemmed miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
title_short miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
title_sort mir-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6176155/
https://www.ncbi.nlm.nih.gov/pubmed/30344679
http://dx.doi.org/10.3892/etm.2018.6679
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