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Biochemical and biophysical research communications. 2025 Apr 26:767:151898. doi: 10.1016/j.bbrc.2025.151898 Q32.22025

Transcription factor BACH1 promotes epithelial-mesenchymal transition by repressing iron metabolism-related genes

转录因子BACH1通过抑制铁代谢相关基因促进上皮间质转化效应 翻译改进

Shuichiro Hayashi  1, Mitsuyo Matsumoto  2, Liang Liu  3, Miho Tanaka  4, Michiaki Unno  5, Kazuhiko Igarashi  6

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作者单位

  • 1 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan; Department of Surgery, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan.
  • 2 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan; Institute of Multidisciplinary Research for Advanced Materials, Tohoku University, Katahira 2-1-1, Sendai, 980-8577, Japan. Electronic address: mitsuyo.matsumoto.d5@tohoku.ac.jp.
  • 3 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan; Developmental Therapeutics Branch, Center for Cancer Research, NCI Bethesda, MD 20892-4264, USA.
  • 4 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan.
  • 5 Department of Surgery, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan.
  • 6 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai, 980-8575, Japan. Electronic address: kazuhiko.igarashi.a5@tohoku.ac.jp.

    • DOI: 10.1016/j.bbrc.2025.151898 PMID: 40315568

    摘要 中英对照阅读

    Pancreatic adenocarcinoma (PDAC) is one of the cancers with a very poor prognosis for its highly invasive and metastatic ability. Epithelial-mesenchymal transition (EMT) is critical for metastasis and invasion of PDAC cells, in which the expression of epithelial genes, such as E-cadherin (CDH1), decreases and that of mesenchymal genes increases. Transcription factor BTB and CNC homology 1 (BACH1) promotes EMT of PDAC cells in part by indirectly suppressing... ...点击完成人机验证后继续浏览

    胰腺导管腺癌（PDAC）是一种预后极差的癌症，因其高度侵袭性和转移能力。上皮-间质转化（EMT）对PDAC细胞的转移和侵袭至关重要，在此过程中，如E-钙粘蛋白（CDH1）等上皮基因表达降低，而间充质基因表达增加。转录因子BTB和CNC同源物1（BACH1）通过间接抑制CDH1的表达在一定程度上促进PDAC细胞发生EMT。然而，其背后的机制尚不清楚。鉴于最近有关细胞内铁与癌细胞中CDH1表达之间联系的报道，我们研究了BACH1是否通过调节铁蛋白基因来抑制CDH1的表达。当用铁螯合剂deferasirox（DFX）处理AsPC-1 PDAC细胞时，CDH1的表达增加。虽然敲除BACH1导致CDH1表达增加，但同时敲除BACH1和铁蛋白重链基因（FTH1）逆转了CDH1的表达。TBK1（BACH1的上游调节因子），在维持AsPC-1细胞中EMT基因表达模式方面是必需的。在SW1990 PDAC细胞中，TBK1与BACH1功能冗余以维持VIM表达，表明其在独立于BACH1的情况下参与了EMT。因此，BACH1对CDH1和EMT的调节涉及铁蛋白FTH1和细胞内铁作为介导物，并且TBK1作为上游和并行调节因子。

    关键词：BACH1；CDH1；上皮-间质转化；铁；胰腺癌；TBK1.

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    Copyright © Biochemical and biophysical research communications. 中文内容为AI机器翻译，仅供参考！

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    期刊名：Biochemical and biophysical research communications

    缩写：BIOCHEM BIOPH RES CO

    ISSN：0006-291X

    e-ISSN：1090-2104

    IF/分区：2.2/Q3

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    Transcription factor BACH1 promotes epithelial-mesenchymal transition by repressing iron metabolism-related genes