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microRNA-1301-mediated inhibition of tumorigenesis
The relatively recent discovery of microRNAs has added a completely new dimension to the study of the regulation of tumor cells, but how they control cell behavior remains largely elusive. HepG2 cells were assigned to the miR-1301 group and the control group. RT-PCR, Western blotting, wound healing,...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583550/ https://www.ncbi.nlm.nih.gov/pubmed/22159405 http://dx.doi.org/10.3892/or.2011.1589 |
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author | FANG, LIN YANG, NING MA, JIE FU, YONG YANG, GUANG-SHUN |
author_facet | FANG, LIN YANG, NING MA, JIE FU, YONG YANG, GUANG-SHUN |
author_sort | FANG, LIN |
collection | PubMed |
description | The relatively recent discovery of microRNAs has added a completely new dimension to the study of the regulation of tumor cells, but how they control cell behavior remains largely elusive. HepG2 cells were assigned to the miR-1301 group and the control group. RT-PCR, Western blotting, wound healing, the Transwell chamber migration and MTT assays, and apoptosis detection assays were used to analyze cell behavior of HepG2 cells after miR-1301 mimic transfection. Our study showed that miR-1301 was downregulated in HepG2 cells, and that miR-1301 inhibited migration and invasion of HepG2 cells and promoted cellular apoptosis after transfection with miR-1301 mimics. In addition, p53 mRNA and p53 protein expression was upregulated, and Bcl-2 and Bcl-xL mRNA and protein expression was downregulated in the miR-1301 group. These results indicate that miR-1301 may be an inhibitor of tumorigenesis in HepG2 cells. |
format | Online Article Text |
id | pubmed-3583550 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-35835502013-02-28 microRNA-1301-mediated inhibition of tumorigenesis FANG, LIN YANG, NING MA, JIE FU, YONG YANG, GUANG-SHUN Oncol Rep Articles The relatively recent discovery of microRNAs has added a completely new dimension to the study of the regulation of tumor cells, but how they control cell behavior remains largely elusive. HepG2 cells were assigned to the miR-1301 group and the control group. RT-PCR, Western blotting, wound healing, the Transwell chamber migration and MTT assays, and apoptosis detection assays were used to analyze cell behavior of HepG2 cells after miR-1301 mimic transfection. Our study showed that miR-1301 was downregulated in HepG2 cells, and that miR-1301 inhibited migration and invasion of HepG2 cells and promoted cellular apoptosis after transfection with miR-1301 mimics. In addition, p53 mRNA and p53 protein expression was upregulated, and Bcl-2 and Bcl-xL mRNA and protein expression was downregulated in the miR-1301 group. These results indicate that miR-1301 may be an inhibitor of tumorigenesis in HepG2 cells. D.A. Spandidos 2011-12-12 2012-04 /pmc/articles/PMC3583550/ /pubmed/22159405 http://dx.doi.org/10.3892/or.2011.1589 Text en Copyright © 2012, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles FANG, LIN YANG, NING MA, JIE FU, YONG YANG, GUANG-SHUN microRNA-1301-mediated inhibition of tumorigenesis |
title | microRNA-1301-mediated inhibition of tumorigenesis |
title_full | microRNA-1301-mediated inhibition of tumorigenesis |
title_fullStr | microRNA-1301-mediated inhibition of tumorigenesis |
title_full_unstemmed | microRNA-1301-mediated inhibition of tumorigenesis |
title_short | microRNA-1301-mediated inhibition of tumorigenesis |
title_sort | microrna-1301-mediated inhibition of tumorigenesis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583550/ https://www.ncbi.nlm.nih.gov/pubmed/22159405 http://dx.doi.org/10.3892/or.2011.1589 |
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