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<p>Pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent and aggressive forms of pancreatic cancer with low survival rates and limited treatment options. Aberrant expression of the <i>MYC</i> oncogene promotes PDAC progression. Recent reports have established a role for enhancer RNAs (eRNAs), originating from active enhancers, in controlling gene transcription. Here we show that a novel <i>MYC</i> eRNA regulates <i>MYC</i> gene expression during chronic inflammatory conditions in pancreatic cancer cells. A higher amount of <i>MYC</i> eRNA is observed in chronic pancreatitis and in pancreatic cancer patients. We show that <i>MYC</i> eRNA interacts with YEATS2, a histone reader protein of the ATAC-HAT complex, and augments the association of YEATS2-containing ATAC complexes with <i>MYC</i> promoter/enhancer regions and thus increases <i>MYC</i> gene expression. TNF-α induced Tyrosine dephosphorylation of the YEATS domain increases <i>MYC</i> eRNA binding to the YEATS2 protein in pancreatic cancer cells. Our study adds another regulatory layer of <i>MYC</i> gene expression by enhancer-driven transcription.</p>

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Dynamic interaction of MYC enhancer RNA with YEATS2 protein regulates MYC gene transcription in pancreatic cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月11日

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  • Jayita Roy,
  • Aniket Kumar,
  • Shouvik Chakravarty,
  • Nidhan K Biswas,
  • Srikanta Goswami,
  • Anup Mazumder

摘要

Pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent and aggressive forms of pancreatic cancer with low survival rates and limited treatment options. Aberrant expression of the MYC oncogene promotes PDAC progression. Recent reports have established a role for enhancer RNAs (eRNAs), originating from active enhancers, in controlling gene transcription. Here we show that a novel MYC eRNA regulates MYC gene expression during chronic inflammatory conditions in pancreatic cancer cells. A higher amount of MYC eRNA is observed in chronic pancreatitis and in pancreatic cancer patients. We show that MYC eRNA interacts with YEATS2, a histone reader protein of the ATAC-HAT complex, and augments the association of YEATS2-containing ATAC complexes with MYC promoter/enhancer regions and thus increases MYC gene expression. TNF-α induced Tyrosine dephosphorylation of the YEATS domain increases MYC eRNA binding to the YEATS2 protein in pancreatic cancer cells. Our study adds another regulatory layer of MYC gene expression by enhancer-driven transcription.