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FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis
The factor that binds to the inducer of short transcripts‐1 (FBI-1) is a transcription suppressor and an important proto‐oncogene that plays multiple roles in carcinogenesis and therapeutic resistance. In the present work, our results indicated that FBI-1 enhanced the resistance of triple-negative b...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7554048/ https://www.ncbi.nlm.nih.gov/pubmed/33051436 http://dx.doi.org/10.1038/s41419-020-03053-0 |
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author | Yang, Hua Ren, Lili Wang, Yanan Bi, Xuebing Li, Xiaoli Wen, Ming Zhang, Qian Yang, Yang Jia, Youchao Li, Yumiao Zang, Aimin wei, Yaning Dai, Guanghai |
author_facet | Yang, Hua Ren, Lili Wang, Yanan Bi, Xuebing Li, Xiaoli Wen, Ming Zhang, Qian Yang, Yang Jia, Youchao Li, Yumiao Zang, Aimin wei, Yaning Dai, Guanghai |
author_sort | Yang, Hua |
collection | PubMed |
description | The factor that binds to the inducer of short transcripts‐1 (FBI-1) is a transcription suppressor and an important proto‐oncogene that plays multiple roles in carcinogenesis and therapeutic resistance. In the present work, our results indicated that FBI-1 enhanced the resistance of triple-negative breast cancer (TNBC) cells to chemotherapeutic agents by repressing the expression of micoRNA-30c targeting the pregnane X receptor (PXR). The expression of FBI-1 was positively related to PXR and its downstream drug resistance-related genes in TNBC tissues. FBI-1 enhanced the expression of PXR and enhanced the activation of the PXR pathway. The miR-30c decreased the expression of PXR by targeting the 3′-UTR of PXR, and FBI-1 increased the expression of PXR by repressing miR-30c’s expression. Through the miR-30c/PXR axis, FBI-1 accelerated the clearance or elimination of antitumor agents in TNBC cells (the TNBC cell lines or the patients derived cells [PDCs]) and induced the resistance of cells to antitumor agents. Therefore, the results indicated that the miR-30c/PXR axis participates in the FBI-1-mediated drug-resistance of TNBC cells. |
format | Online Article Text |
id | pubmed-7554048 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-75540482020-10-19 FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis Yang, Hua Ren, Lili Wang, Yanan Bi, Xuebing Li, Xiaoli Wen, Ming Zhang, Qian Yang, Yang Jia, Youchao Li, Yumiao Zang, Aimin wei, Yaning Dai, Guanghai Cell Death Dis Article The factor that binds to the inducer of short transcripts‐1 (FBI-1) is a transcription suppressor and an important proto‐oncogene that plays multiple roles in carcinogenesis and therapeutic resistance. In the present work, our results indicated that FBI-1 enhanced the resistance of triple-negative breast cancer (TNBC) cells to chemotherapeutic agents by repressing the expression of micoRNA-30c targeting the pregnane X receptor (PXR). The expression of FBI-1 was positively related to PXR and its downstream drug resistance-related genes in TNBC tissues. FBI-1 enhanced the expression of PXR and enhanced the activation of the PXR pathway. The miR-30c decreased the expression of PXR by targeting the 3′-UTR of PXR, and FBI-1 increased the expression of PXR by repressing miR-30c’s expression. Through the miR-30c/PXR axis, FBI-1 accelerated the clearance or elimination of antitumor agents in TNBC cells (the TNBC cell lines or the patients derived cells [PDCs]) and induced the resistance of cells to antitumor agents. Therefore, the results indicated that the miR-30c/PXR axis participates in the FBI-1-mediated drug-resistance of TNBC cells. Nature Publishing Group UK 2020-10-13 /pmc/articles/PMC7554048/ /pubmed/33051436 http://dx.doi.org/10.1038/s41419-020-03053-0 Text en © The Author(s) 2020 Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Yang, Hua Ren, Lili Wang, Yanan Bi, Xuebing Li, Xiaoli Wen, Ming Zhang, Qian Yang, Yang Jia, Youchao Li, Yumiao Zang, Aimin wei, Yaning Dai, Guanghai FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis |
title | FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis |
title_full | FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis |
title_fullStr | FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis |
title_full_unstemmed | FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis |
title_short | FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis |
title_sort | fbi-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the mir-30c/pxr axis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7554048/ https://www.ncbi.nlm.nih.gov/pubmed/33051436 http://dx.doi.org/10.1038/s41419-020-03053-0 |
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