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miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway
BACKGROUND: The function of miR‐138‐5p as an oncogenic factor has been reported in certain cancers. This study was performed to analyze the potential involvement of miR‐138‐5p in kidney renal clear cell carcinoma (KIRC). METHODS: The Cancer Genome Atlas (TCGA) database was used to explain the expres...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8605131/ https://www.ncbi.nlm.nih.gov/pubmed/34586647 http://dx.doi.org/10.1002/jcla.23766 |
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author | Liu, Yang Qu, Hong‐chen |
author_facet | Liu, Yang Qu, Hong‐chen |
author_sort | Liu, Yang |
collection | PubMed |
description | BACKGROUND: The function of miR‐138‐5p as an oncogenic factor has been reported in certain cancers. This study was performed to analyze the potential involvement of miR‐138‐5p in kidney renal clear cell carcinoma (KIRC). METHODS: The Cancer Genome Atlas (TCGA) database was used to explain the expression of miR‐138‐5p in cancer and paired non‐cancer tissues of KIRC patients. Subsequently, miR‐138‐5p expression in KIRC tissues and cell lines, as well as that in normal tissues and normal renal tubular epithelial cell line, was detected. Artificial overexpressing of miR‐138‐5p was applied to observe its effect on the biological behaviors of KIRC cells. The target mRNA of miR‐138‐5p, SIN3A, was predicted and validated. Altered expression of miR‐138‐5p and SIN3A was introduced to confirm their functions in KIRC proliferation and invasion. RESULTS: We showed that miR‐138‐5p was down‐regulated in tumor tissues of KIRC patients comparing to adjacent healthy tissues and linked to dismal prognosis in patients. miR‐138‐5p could hinder KIRC proliferation and invasion, while artificial overexpression of SIN3A led to reversed trends. SIN3A was a target mRNA of miR‐138‐5p. miR‐138‐5p and SIN3A together affect the activation of the Notch signaling pathway. CONCLUSION: This study evidenced that up‐regulated miR‐138‐5p inhibits proliferation and invasion of KIRC cells involving the transcription of SIN3A and the following regulation of the Notch signaling pathway. |
format | Online Article Text |
id | pubmed-8605131 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86051312021-11-24 miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway Liu, Yang Qu, Hong‐chen J Clin Lab Anal Research Articles BACKGROUND: The function of miR‐138‐5p as an oncogenic factor has been reported in certain cancers. This study was performed to analyze the potential involvement of miR‐138‐5p in kidney renal clear cell carcinoma (KIRC). METHODS: The Cancer Genome Atlas (TCGA) database was used to explain the expression of miR‐138‐5p in cancer and paired non‐cancer tissues of KIRC patients. Subsequently, miR‐138‐5p expression in KIRC tissues and cell lines, as well as that in normal tissues and normal renal tubular epithelial cell line, was detected. Artificial overexpressing of miR‐138‐5p was applied to observe its effect on the biological behaviors of KIRC cells. The target mRNA of miR‐138‐5p, SIN3A, was predicted and validated. Altered expression of miR‐138‐5p and SIN3A was introduced to confirm their functions in KIRC proliferation and invasion. RESULTS: We showed that miR‐138‐5p was down‐regulated in tumor tissues of KIRC patients comparing to adjacent healthy tissues and linked to dismal prognosis in patients. miR‐138‐5p could hinder KIRC proliferation and invasion, while artificial overexpression of SIN3A led to reversed trends. SIN3A was a target mRNA of miR‐138‐5p. miR‐138‐5p and SIN3A together affect the activation of the Notch signaling pathway. CONCLUSION: This study evidenced that up‐regulated miR‐138‐5p inhibits proliferation and invasion of KIRC cells involving the transcription of SIN3A and the following regulation of the Notch signaling pathway. John Wiley and Sons Inc. 2021-09-29 /pmc/articles/PMC8605131/ /pubmed/34586647 http://dx.doi.org/10.1002/jcla.23766 Text en © 2021 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Liu, Yang Qu, Hong‐chen miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway |
title | miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway |
title_full | miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway |
title_fullStr | miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway |
title_full_unstemmed | miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway |
title_short | miR‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting SINA3 and regulation of the Notch signaling pathway |
title_sort | mir‐138‐5p inhibits proliferation and invasion in kidney renal clear cell carcinoma by targeting sina3 and regulation of the notch signaling pathway |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8605131/ https://www.ncbi.nlm.nih.gov/pubmed/34586647 http://dx.doi.org/10.1002/jcla.23766 |
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