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MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells
MicroRNAs (miRs) have shown tremendous potential to act as therapeutic targets for cancer treatment. In this context, the present study was designed to investigate the potential of miR-143 in the treatment of breast cancer. Results showed that miR-143 to be significantly (P < 0.05) downregulated...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394972/ https://www.ncbi.nlm.nih.gov/pubmed/32737620 http://dx.doi.org/10.1186/s13568-020-01072-w |
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author | Du, Yiqun Zhang, Jian Meng, Yanchun Huang, Mingzhu Yan, Wangjun Wu, Zhiqiang |
author_facet | Du, Yiqun Zhang, Jian Meng, Yanchun Huang, Mingzhu Yan, Wangjun Wu, Zhiqiang |
author_sort | Du, Yiqun |
collection | PubMed |
description | MicroRNAs (miRs) have shown tremendous potential to act as therapeutic targets for cancer treatment. In this context, the present study was designed to investigate the potential of miR-143 in the treatment of breast cancer. Results showed that miR-143 to be significantly (P < 0.05) downregulated in breast cancer tissues and cell lines. The miR-143 has inhibitory effect on CAMA-1cell growth which was manifested as significant (P < 0.05) decline in loss of viability of cancer cells. The loss of cell viability was revealed to be due to the induction of apoptotic cell death as evident from acridine orange/ethidium bromide (AO/EB) and 4′,6-diamidino-2-phenylindole (DAPI) staining assays. The apoptotic cell percentage was found to be 35.7% in miR-143 mimics transfected in comparison to 6.4% in miR-NC transfected cells. The western blot analysis showed that miR-143 caused enhancement in Bax and suppression in Bcl-2 expression in CAMA-1 cells. The miR-143 also suppressed the bone metastasis of the CAMA-1 cells by suppressing the expression of Jag1 and deactivation of the Rho-signalling pathway. The transwell assays also showed considerable anti-metastatic effects of miR-143 on CAMA-1 cells. Taken together, miR-143 has growth inhibitory anti-metastatic effect on breast cancer and thus may prove beneficial in breast cancer treatment. |
format | Online Article Text |
id | pubmed-7394972 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-73949722020-08-18 MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells Du, Yiqun Zhang, Jian Meng, Yanchun Huang, Mingzhu Yan, Wangjun Wu, Zhiqiang AMB Express Original Article MicroRNAs (miRs) have shown tremendous potential to act as therapeutic targets for cancer treatment. In this context, the present study was designed to investigate the potential of miR-143 in the treatment of breast cancer. Results showed that miR-143 to be significantly (P < 0.05) downregulated in breast cancer tissues and cell lines. The miR-143 has inhibitory effect on CAMA-1cell growth which was manifested as significant (P < 0.05) decline in loss of viability of cancer cells. The loss of cell viability was revealed to be due to the induction of apoptotic cell death as evident from acridine orange/ethidium bromide (AO/EB) and 4′,6-diamidino-2-phenylindole (DAPI) staining assays. The apoptotic cell percentage was found to be 35.7% in miR-143 mimics transfected in comparison to 6.4% in miR-NC transfected cells. The western blot analysis showed that miR-143 caused enhancement in Bax and suppression in Bcl-2 expression in CAMA-1 cells. The miR-143 also suppressed the bone metastasis of the CAMA-1 cells by suppressing the expression of Jag1 and deactivation of the Rho-signalling pathway. The transwell assays also showed considerable anti-metastatic effects of miR-143 on CAMA-1 cells. Taken together, miR-143 has growth inhibitory anti-metastatic effect on breast cancer and thus may prove beneficial in breast cancer treatment. Springer Berlin Heidelberg 2020-07-31 /pmc/articles/PMC7394972/ /pubmed/32737620 http://dx.doi.org/10.1186/s13568-020-01072-w Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Original Article Du, Yiqun Zhang, Jian Meng, Yanchun Huang, Mingzhu Yan, Wangjun Wu, Zhiqiang MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells |
title | MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells |
title_full | MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells |
title_fullStr | MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells |
title_full_unstemmed | MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells |
title_short | MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells |
title_sort | microrna-143 targets mapk3 to regulate the proliferation and bone metastasis of human breast cancer cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394972/ https://www.ncbi.nlm.nih.gov/pubmed/32737620 http://dx.doi.org/10.1186/s13568-020-01072-w |
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