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KMT2D-mediated H3K4me1 recruits YBX1 to facilitate triple-negative breast cancer progression through epigenetic activation of c-Myc.

Bing YaoMengying XingXiangwei ZengMing ZhangQue ZhengZhi WangBo PengShuang QuLingyun LiYucui JinHaitao LiHongyan YuanQuan ZhaoChangyan Ma
Published in: Clinical and translational medicine (2024)
YBX1 is a KMT2D-mediated H3K4me1-binding effector protein and mutation of YBX1 (E121A) disrupts its binding to H3K4me1. KMT2D and YBX1 cooperatively promote TNBC proliferation and metastasis by activating c-Myc and SENP1 expression in vitro and in vivo. YBX1 is colocalized with H3K4me1 in the c-Myc and SENP1 promoter regions in TNBC cells and increased YBX1 expression predicts a poor prognosis in breast cancer patients.
Keyphrases
  • poor prognosis
  • long non coding rna
  • dna methylation
  • signaling pathway
  • gene expression
  • induced apoptosis
  • transcription factor
  • cell cycle arrest
  • cell proliferation
  • oxidative stress
  • cell death
  • amino acid