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Updated: Jan 9, 2026

In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
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In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability

Published on: October 19, 2018

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c-Myc-PANK3-EMT axis regulates the structure and function of intestinal barrier in ulcerative colitis

Shize Zhang1, Yuang Chen1, Nan Aa2

  • 1Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, PR China.

Journal of Advanced Research
|December 10, 2025
PubMed
Abstract

Insights

Researchers identified Pantothenate Kinase 3 (PANK3) as crucial for intestinal barrier repair in ulcerative colitis (UC). Folic acid acts as a PANK3 agonist, offering a potential therapeutic strategy for UC by restoring barrier function.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Drug Discovery

Background:

  • Intestinal barrier damage is critical in ulcerative colitis (UC) pathogenesis.
  • Effective therapeutic targets for UC-induced barrier repair are currently lacking.

Purpose of the Study:

  • To explore mechanisms underlying intestinal barrier repair in UC.
  • To identify novel therapeutic targets for UC.

Main Methods:

  • Nontargeted metabolomic and transcriptomic analyses were performed on DSS-induced colitis models.
  • Pantothenate kinase 3 (PANK3) was modulated genetically and pharmacologically.
  • Upstream regulators and downstream effects of PANK3, including the c-Myc-PANK3-EMT axis, were investigated.
  • PANK3 agonists were screened and validated in vitro and in vivo.

Main Results:

  • Decreased PANK3 expression was observed in human UC patients and murine colitis models.
  • PANK3 activation or overexpression restored intestinal barrier integrity in UC mice.
  • PANK3 negatively regulates epithelial-mesenchymal transition (EMT) via the c-Myc pathway.
  • Folic acid was identified as a PANK3 agonist that improves intestinal barrier function in DSS-induced colitis.

Conclusions:

  • The c-Myc-PANK3-EMT axis is vital for maintaining intestinal barrier structure and function.
  • PANK3 represents a potential therapeutic target for UC.
  • Folic acid is a promising candidate agonist for repairing the intestinal barrier in UC.
Keywords:
EMTFolic acidIntestinal barrierPANK3Ulcerative colitisc-Myc

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