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MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α

The proliferation and apoptosis of tumor cells are regulated by a variety of microRNAs (miRs). miR-21 can inhibit the apoptosis of cancer cells in vitro. Tumor necrosis factor α (TNF-α) serves an important role in the induction of proliferation of cervical cancer cells. Previous studies have demonst...

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Autores principales: Xu, Lin, Xu, Qian, Li, Xiwen, Zhang, Xiaoling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647022/
https://www.ncbi.nlm.nih.gov/pubmed/28765959
http://dx.doi.org/10.3892/mmr.2017.7143
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author Xu, Lin
Xu, Qian
Li, Xiwen
Zhang, Xiaoling
author_facet Xu, Lin
Xu, Qian
Li, Xiwen
Zhang, Xiaoling
author_sort Xu, Lin
collection PubMed
description The proliferation and apoptosis of tumor cells are regulated by a variety of microRNAs (miRs). miR-21 can inhibit the apoptosis of cancer cells in vitro. Tumor necrosis factor α (TNF-α) serves an important role in the induction of proliferation of cervical cancer cells. Previous studies have demonstrated that the expression level of miR-21 is associated with TNF-α expression in alveolar macrophages. However, to the best of our knowledge, whether miR-21 regulates TNF-α in cervical cells has not been reported. The present study was designed to investigate whether miR-21 regulates TNF-α expression, proliferation and apoptosis of cervical cancer cells. miR-21, miR-21 inhibitor and control miRNA were synthesized and transfected into HeLa cervical cancer cells. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression levels of miR-21 and TNF-α at the mRNA level. Western blotting was used to measure the expression levels of TNF-α at the protein level. MTT assay and Hoechest-33342 staining were used to measure the proliferation and apoptosis of HeLa cells. miR-21 was identified to upregulate the mRNA and protein expression levels of TNF-α. Furthermore, upregulation of TNF-α enhanced the proliferation capability of HeLa cells. Changes in the expression levels of miR-21 and TNF-α did not significantly affect the apoptosis of Hela cells. In conclusion, the present study demonstrated that miR-21 regulates the expression of TNF-α in HeLa cells. Additionally, the expression level of TNF-α was positively associated with the proliferation capability of Hela cells, but not apoptosis. Therefore, miR-21 regulates the proliferation of HeLa cells through regulation of TNF-α. These results provide novel potential therapeutic targets for the treatment of cervical cancer.
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spelling pubmed-56470222017-10-24 MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α Xu, Lin Xu, Qian Li, Xiwen Zhang, Xiaoling Mol Med Rep Articles The proliferation and apoptosis of tumor cells are regulated by a variety of microRNAs (miRs). miR-21 can inhibit the apoptosis of cancer cells in vitro. Tumor necrosis factor α (TNF-α) serves an important role in the induction of proliferation of cervical cancer cells. Previous studies have demonstrated that the expression level of miR-21 is associated with TNF-α expression in alveolar macrophages. However, to the best of our knowledge, whether miR-21 regulates TNF-α in cervical cells has not been reported. The present study was designed to investigate whether miR-21 regulates TNF-α expression, proliferation and apoptosis of cervical cancer cells. miR-21, miR-21 inhibitor and control miRNA were synthesized and transfected into HeLa cervical cancer cells. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression levels of miR-21 and TNF-α at the mRNA level. Western blotting was used to measure the expression levels of TNF-α at the protein level. MTT assay and Hoechest-33342 staining were used to measure the proliferation and apoptosis of HeLa cells. miR-21 was identified to upregulate the mRNA and protein expression levels of TNF-α. Furthermore, upregulation of TNF-α enhanced the proliferation capability of HeLa cells. Changes in the expression levels of miR-21 and TNF-α did not significantly affect the apoptosis of Hela cells. In conclusion, the present study demonstrated that miR-21 regulates the expression of TNF-α in HeLa cells. Additionally, the expression level of TNF-α was positively associated with the proliferation capability of Hela cells, but not apoptosis. Therefore, miR-21 regulates the proliferation of HeLa cells through regulation of TNF-α. These results provide novel potential therapeutic targets for the treatment of cervical cancer. D.A. Spandidos 2017-10 2017-08-02 /pmc/articles/PMC5647022/ /pubmed/28765959 http://dx.doi.org/10.3892/mmr.2017.7143 Text en Copyright: © Xu 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
Xu, Lin
Xu, Qian
Li, Xiwen
Zhang, Xiaoling
MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
title MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
title_full MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
title_fullStr MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
title_full_unstemmed MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
title_short MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
title_sort microrna-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647022/
https://www.ncbi.nlm.nih.gov/pubmed/28765959
http://dx.doi.org/10.3892/mmr.2017.7143
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