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MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation

The present study aimed to investigate whether microRNA (miR)-490-3p can regulate MAPK1 expression, increase proliferation of esophageal squamous cell carcinoma (ESCC) and reduce ESCC cell apoptosis. The Cancer Genome Atlas (TCGA) database was used to explore the functional role of miR-490-3p in ESC...

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Autores principales: Zabihula, Baerxiaguli, Yiliyasi, Mukedaisi, Lu, Yanrong, Salai, Adili
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676399/
https://www.ncbi.nlm.nih.gov/pubmed/31452793
http://dx.doi.org/10.3892/ol.2019.10636
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author Zabihula, Baerxiaguli
Yiliyasi, Mukedaisi
Lu, Yanrong
Salai, Adili
author_facet Zabihula, Baerxiaguli
Yiliyasi, Mukedaisi
Lu, Yanrong
Salai, Adili
author_sort Zabihula, Baerxiaguli
collection PubMed
description The present study aimed to investigate whether microRNA (miR)-490-3p can regulate MAPK1 expression, increase proliferation of esophageal squamous cell carcinoma (ESCC) and reduce ESCC cell apoptosis. The Cancer Genome Atlas (TCGA) database was used to explore the functional role of miR-490-3p in ESCC. The expression of miR-490-3p in ESCC tissues and adjacent tissues of patients with ESCC were detected by reverse transcription-quantitative PCR. The effect of miR-490-3p on ESCC cell proliferation and apoptosis were detected by cell counting kit-8 and clone formation assay, and flow cytometry, respectively. The dual luciferase reporter assay was used for detect the regulatory association between miR-490-3p and MAPK1. The TCGA dataset demonstrated that miR-490-3p expression was reduced in ESCC tissues compared with normal tissue. The expression of miR-490-3p was also lower in ESCC tissues compared with adjacent tissues. The expression of miR-490-3p in patients with stage III and IV ESCC were significantly lower than those in stage I and II. In patients with tumor >3 cm, miR-490-3p expression was lower than in patients with tumor <3 cm. Gene set enrichment analysis demonstrated that miR-490-3p may essentially regulate cell apoptosis. In addition, miR-490-3p depletion in TE1 and ECA109 cell lines promoted cell proliferation and inhibited cell apoptosis. The results from dual luciferase reporter assay demonstrated that miR-490-3p may be able to degrade MAPK1. Furthermore, MAPK1 overexpression in TE1 and ECA109 cells partially reversed the effects of miR-490-3p on cell proliferation and apoptosis. Low expression of miR-490-3p may therefore promote the proliferation and inhibit the apoptosis of ESCC cells by regulating MAPK1.
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spelling pubmed-66763992019-08-26 MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation Zabihula, Baerxiaguli Yiliyasi, Mukedaisi Lu, Yanrong Salai, Adili Oncol Lett Articles The present study aimed to investigate whether microRNA (miR)-490-3p can regulate MAPK1 expression, increase proliferation of esophageal squamous cell carcinoma (ESCC) and reduce ESCC cell apoptosis. The Cancer Genome Atlas (TCGA) database was used to explore the functional role of miR-490-3p in ESCC. The expression of miR-490-3p in ESCC tissues and adjacent tissues of patients with ESCC were detected by reverse transcription-quantitative PCR. The effect of miR-490-3p on ESCC cell proliferation and apoptosis were detected by cell counting kit-8 and clone formation assay, and flow cytometry, respectively. The dual luciferase reporter assay was used for detect the regulatory association between miR-490-3p and MAPK1. The TCGA dataset demonstrated that miR-490-3p expression was reduced in ESCC tissues compared with normal tissue. The expression of miR-490-3p was also lower in ESCC tissues compared with adjacent tissues. The expression of miR-490-3p in patients with stage III and IV ESCC were significantly lower than those in stage I and II. In patients with tumor >3 cm, miR-490-3p expression was lower than in patients with tumor <3 cm. Gene set enrichment analysis demonstrated that miR-490-3p may essentially regulate cell apoptosis. In addition, miR-490-3p depletion in TE1 and ECA109 cell lines promoted cell proliferation and inhibited cell apoptosis. The results from dual luciferase reporter assay demonstrated that miR-490-3p may be able to degrade MAPK1. Furthermore, MAPK1 overexpression in TE1 and ECA109 cells partially reversed the effects of miR-490-3p on cell proliferation and apoptosis. Low expression of miR-490-3p may therefore promote the proliferation and inhibit the apoptosis of ESCC cells by regulating MAPK1. D.A. Spandidos 2019-09 2019-07-18 /pmc/articles/PMC6676399/ /pubmed/31452793 http://dx.doi.org/10.3892/ol.2019.10636 Text en Copyright: © Zabihula 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
Zabihula, Baerxiaguli
Yiliyasi, Mukedaisi
Lu, Yanrong
Salai, Adili
MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation
title MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation
title_full MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation
title_fullStr MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation
title_full_unstemmed MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation
title_short MicroRNA-490-3p inhibits proliferation and stimulates apoptosis of ESCC cells via MAPK1 downregulation
title_sort microrna-490-3p inhibits proliferation and stimulates apoptosis of escc cells via mapk1 downregulation
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676399/
https://www.ncbi.nlm.nih.gov/pubmed/31452793
http://dx.doi.org/10.3892/ol.2019.10636
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