Literature DB >> 33051436

FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis.

Hua Yang1,2, Lili Ren2, Yanan Wang2, Xuebing Bi2, Xiaoli Li2, Ming Wen3, Qian Zhang2, Yang Yang2, Youchao Jia2, Yumiao Li2, Aimin Zang2, Yaning Wei4, Guanghai Dai5.   

Abstract

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.

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Year:  2020        PMID: 33051436      PMCID: PMC7554048          DOI: 10.1038/s41419-020-03053-0

Source DB:  PubMed          Journal:  Cell Death Dis            Impact factor:   8.469


  57 in total

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