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MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis
Introduction: MicroRNAs (miRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) via modulating expression of their targeting mRNAs. The present study aimed to investigate the role of miR-1205 in HCC cell proliferation and investigate the underlying molecular mechanism. Met...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834419/ https://www.ncbi.nlm.nih.gov/pubmed/36617978 http://dx.doi.org/10.1177/15330338221150544 |
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author | Li, Xiang Xie, Shujie Xia, Qin Yan, Jia Chen, Shuhuai Shen, Jia |
author_facet | Li, Xiang Xie, Shujie Xia, Qin Yan, Jia Chen, Shuhuai Shen, Jia |
author_sort | Li, Xiang |
collection | PubMed |
description | Introduction: MicroRNAs (miRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) via modulating expression of their targeting mRNAs. The present study aimed to investigate the role of miR-1205 in HCC cell proliferation and investigate the underlying molecular mechanism. Methods: The effects of miR-1205 on proliferation ability of HCC cell lines were explored in vitro and in vivo. Real-time quantitative PCR (qPCR) analysis was performed to determine miR-1205 expression in HCC tissues and cell lines. Online prediction tools and luciferase assays were used to identify potential target genes of miR-1205. Western blot analysis and dual-luciferase assays were conducted to screen key signaling pathway proteins regulated by miR-1205 and its’ target gene. Results: In vitro and in vivo experiments showed that miR-1205 inhibits the proliferation of HCC cells. Dual-luciferase assays showed that miR-1205 interacted with CSNK2B by directly targeting the miRNA-binding site in the CSNK2B sequence, and further qPCR analysis indicated that CSNK2B expression was increased in HCC tissues and negatively correlated with miR-1205 expression. Furthermore, CSNK2B significantly promoted HCC cell proliferation, and CSNK2B overexpression or knockdown attenuated the effects of miR-1205 overexpression or inhibition on HCC cell viability, respectively. Mechanistically, miR-1205 suppresses HCC cell proliferation via a CSNK2B/CDK4 axis. Conclusion: The present results indicated that miR-1205 suppressed HCC cell proliferation by directly targeting CSNK2B and thus inhibiting the CDK4/pRb cell cycle pathway. |
format | Online Article Text |
id | pubmed-9834419 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-98344192023-01-13 MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis Li, Xiang Xie, Shujie Xia, Qin Yan, Jia Chen, Shuhuai Shen, Jia Technol Cancer Res Treat Original Article Introduction: MicroRNAs (miRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) via modulating expression of their targeting mRNAs. The present study aimed to investigate the role of miR-1205 in HCC cell proliferation and investigate the underlying molecular mechanism. Methods: The effects of miR-1205 on proliferation ability of HCC cell lines were explored in vitro and in vivo. Real-time quantitative PCR (qPCR) analysis was performed to determine miR-1205 expression in HCC tissues and cell lines. Online prediction tools and luciferase assays were used to identify potential target genes of miR-1205. Western blot analysis and dual-luciferase assays were conducted to screen key signaling pathway proteins regulated by miR-1205 and its’ target gene. Results: In vitro and in vivo experiments showed that miR-1205 inhibits the proliferation of HCC cells. Dual-luciferase assays showed that miR-1205 interacted with CSNK2B by directly targeting the miRNA-binding site in the CSNK2B sequence, and further qPCR analysis indicated that CSNK2B expression was increased in HCC tissues and negatively correlated with miR-1205 expression. Furthermore, CSNK2B significantly promoted HCC cell proliferation, and CSNK2B overexpression or knockdown attenuated the effects of miR-1205 overexpression or inhibition on HCC cell viability, respectively. Mechanistically, miR-1205 suppresses HCC cell proliferation via a CSNK2B/CDK4 axis. Conclusion: The present results indicated that miR-1205 suppressed HCC cell proliferation by directly targeting CSNK2B and thus inhibiting the CDK4/pRb cell cycle pathway. SAGE Publications 2023-01-09 /pmc/articles/PMC9834419/ /pubmed/36617978 http://dx.doi.org/10.1177/15330338221150544 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Li, Xiang Xie, Shujie Xia, Qin Yan, Jia Chen, Shuhuai Shen, Jia MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis |
title | MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis |
title_full | MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis |
title_fullStr | MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis |
title_full_unstemmed | MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis |
title_short | MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis |
title_sort | microrna-1205 suppresses hepatocellular carcinoma cell proliferation via a csnk2b/cdk4 axis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834419/ https://www.ncbi.nlm.nih.gov/pubmed/36617978 http://dx.doi.org/10.1177/15330338221150544 |
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