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<p>Colorectal cancer (CRC) progression is associated with intestinal barrier dysfunction, yet the molecular mechanisms governing mucin glycosylation remain unclear. This study aims to investigate the regulatory pathway controlling MUC2 expression and O-glycosylation in CRC and assess the therapeutic potential of rosiglitazone in restoring mucosal integrity. In this study, B3GNT6 was identified as a key glycosyltransferase that promotes MUC2 O-glycosylation and protein stability. KLF4 was shown to transcriptionally regulate both B3GNT6 and MUC2, with its activity modulated by PPARg. Treatment with the PPARg agonist rosiglitazone activated the PPARg-KLF4-B3GNT6 axis, restoring MUC2 function and enhancing the mucus barrier integrity. These findings highlight a novel therapeutic avenue for CRC by targeting mucin glycosylation.</p><p></p>

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Restoring O-glycosylation and expression of MUC2 limits progression of colorectal cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月21日

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  • Yian Yang,
  • Yuesong Yin,
  • Wei Xu,
  • Yan Kang,
  • Jiawei Chen,
  • Yanfeng Zou,
  • Xuan Wang,
  • Zhigang Xiao,
  • Peiguo Cao,
  • Zheng Li

摘要

Colorectal cancer (CRC) progression is associated with intestinal barrier dysfunction, yet the molecular mechanisms governing mucin glycosylation remain unclear. This study aims to investigate the regulatory pathway controlling MUC2 expression and O-glycosylation in CRC and assess the therapeutic potential of rosiglitazone in restoring mucosal integrity. In this study, B3GNT6 was identified as a key glycosyltransferase that promotes MUC2 O-glycosylation and protein stability. KLF4 was shown to transcriptionally regulate both B3GNT6 and MUC2, with its activity modulated by PPARg. Treatment with the PPARg agonist rosiglitazone activated the PPARg-KLF4-B3GNT6 axis, restoring MUC2 function and enhancing the mucus barrier integrity. These findings highlight a novel therapeutic avenue for CRC by targeting mucin glycosylation.