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Background <p>Biliary atresia (BA) is a severe neonatal disease characterized by obstruction of the biliary system and hepatic fibrosis. Epithelial-mesenchymal transition (EMT) occurs during the development of liver fibrosis in BA. However, the molecular mechanism that promotes elevated MMP7 expression and mediates the EMT process remains unknown. SULT2B1 has been shown to be involved in the intrahepatocellular EMT process, but its role in BA remains unknown.</p> Methods <p>In this study, we found that SULT2B1 was overexpressed in BA livers. The increased expression of SULT2B1 exhibited a high association with the severity of fibrosis and poor prognosis in BA, and it was significantly correlated with the MMP7-mediated EMT in cholangiocytes. Further study showed that the abnormal high expression of SULT2B1 was located in cholangiocytes in BA, which was consistent with the pattern of MMP7. In vitro, upon the treatment of TGF-β1, SULT2B1 was overexpressed and promoted the EMT process via the Wnt/β-catenin/MMP7 pathway in a human intrahepatic bile duct epithelial cell line. Silencing of SULT2B1 expression blocked Wnt/β-catenin/MMP7-mediated cholangiocyte EMT.</p> Results <p>SULT2B1 was overexpressed in BA livers and correlated with fibrosis severity and poor prognosis. Its expression was associated with MMP7-mediated EMT in cholangiocytes, with overexpression localized similarly to MMP7. TGF-β1 induced SULT2B1 overexpression, activating the Wnt/β-catenin/MMP7 pathway to promote EMT, while SULT2B1 silencing inhibited this process.</p> Conclusion <p>Inhibition of the SULT2B1/Wnt/β-catenin/MMP7 axis may represent a potential therapeutic strategy for BA.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>EMT of cholangiocytes in BA is an important process in the development of biliary obstruction and liver fibrosis.</p> </ItemContent> <ItemContent> <p>SULT2B1 was a key molecule involved in regulating cholangiocyte EMT and liver fibrosis processes in BA.</p> </ItemContent> <ItemContent> <p>SULT2B1 induced by TGF-β1 up-regulated MMP7 and promoted EMT in Cholangiocytes.</p> </ItemContent> <ItemContent> <p>Blockage of the SULT2B1/Wnt/β-catenin/MMP7 axis may be a new therapeutic strategy to relieve BA liver fibrosis.</p> </ItemContent> </UnorderedList></p> <p></p>

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SULT2B1 promotes cholangiocyte epithelial-mesenchymal transition via Wnt/β-catenin/MMP7 pathway in biliary atresia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月16日

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  • Ting Yang,
  • Shen Yang,
  • Wenjun Mou,
  • Jiawei Zhao,
  • Huanmin Wang,
  • Yajun Chen,
  • Li Zhang,
  • Libing Fu,
  • Dingding Wang,
  • Jinshi Huang

摘要

Background

Biliary atresia (BA) is a severe neonatal disease characterized by obstruction of the biliary system and hepatic fibrosis. Epithelial-mesenchymal transition (EMT) occurs during the development of liver fibrosis in BA. However, the molecular mechanism that promotes elevated MMP7 expression and mediates the EMT process remains unknown. SULT2B1 has been shown to be involved in the intrahepatocellular EMT process, but its role in BA remains unknown.

Methods

In this study, we found that SULT2B1 was overexpressed in BA livers. The increased expression of SULT2B1 exhibited a high association with the severity of fibrosis and poor prognosis in BA, and it was significantly correlated with the MMP7-mediated EMT in cholangiocytes. Further study showed that the abnormal high expression of SULT2B1 was located in cholangiocytes in BA, which was consistent with the pattern of MMP7. In vitro, upon the treatment of TGF-β1, SULT2B1 was overexpressed and promoted the EMT process via the Wnt/β-catenin/MMP7 pathway in a human intrahepatic bile duct epithelial cell line. Silencing of SULT2B1 expression blocked Wnt/β-catenin/MMP7-mediated cholangiocyte EMT.

Results

SULT2B1 was overexpressed in BA livers and correlated with fibrosis severity and poor prognosis. Its expression was associated with MMP7-mediated EMT in cholangiocytes, with overexpression localized similarly to MMP7. TGF-β1 induced SULT2B1 overexpression, activating the Wnt/β-catenin/MMP7 pathway to promote EMT, while SULT2B1 silencing inhibited this process.

Conclusion

Inhibition of the SULT2B1/Wnt/β-catenin/MMP7 axis may represent a potential therapeutic strategy for BA.

Impact

EMT of cholangiocytes in BA is an important process in the development of biliary obstruction and liver fibrosis.

SULT2B1 was a key molecule involved in regulating cholangiocyte EMT and liver fibrosis processes in BA.

SULT2B1 induced by TGF-β1 up-regulated MMP7 and promoted EMT in Cholangiocytes.

Blockage of the SULT2B1/Wnt/β-catenin/MMP7 axis may be a new therapeutic strategy to relieve BA liver fibrosis.