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USP38 regulates autophagy-dependent ferroptosis by deubiquitinating CTNNB1 in melanoma.

Xin Chu1, Wenjin Wang2

  • 1Department of Dermatology, First Affiliated Hospital of Nanchang University, Nanchang, China.

International Journal of Biological Macromolecules
|December 17, 2025
PubMed
Summary

Ubiquitin-specific protease 38 (USP38) drives melanoma progression by stabilizing Catenin Beta 1 (CTNNB1), suppressing ferroptosis. Targeting this USP38-CTNNB1 pathway offers a promising therapeutic strategy for melanoma.

Keywords:
AutophagyFerroptosisMelanomaUSP38Ubiquitination

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Melanoma incidence is rising, posing clinical challenges.
  • The role of Ubiquitin-specific protease 38 (USP38) in melanoma progression is unclear.
  • USP38 is implicated in tumor progression across various cancers.

Purpose of the Study:

  • To elucidate the mechanism of USP38 in melanoma.
  • To investigate USP38's role in melanoma cell proliferation, migration, epithelial-mesenchymal transition, and ferroptosis.
  • To identify therapeutic targets within the USP38 pathway.

Main Methods:

  • Analysis of USP38 expression in human melanoma tissues.
  • In vitro studies on melanoma cell proliferation, migration, and ferroptosis.
  • In vivo and in vitro experiments involving USP38 and Catenin Beta 1 (CTNNB1) manipulation.
  • Autophagy inhibition and ferroptosis induction assays.
  • Ubiquitination assays and Western blotting.

Main Results:

  • USP38 is overexpressed in melanoma tissues and promotes proliferation, migration, and EMT while suppressing ferroptosis.
  • USP38 knockdown inhibits growth, activates autophagy-dependent ferroptosis, and stabilizes CTNNB1 by removing K48-linked ubiquitination.
  • CTNNB1 knockdown reverses USP38-driven tumor progression.
  • Combined USP38 knockdown and CTNNB1 degrader NF764 synergistically suppress tumor growth and induce ferroptosis.

Conclusions:

  • USP38 drives melanoma progression and suppresses ferroptosis via CTNNB1 stabilization and autophagy.
  • Targeting the USP38-CTNNB1 axis is a potential therapeutic strategy for melanoma.
  • USP38 regulates autophagy-dependent ferroptosis in melanoma.