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The Cx43-Mediated Autophagy Mechanism Influences Triple-Negative Breast Cancer Through the Regulation of Rab31
Jiao Yang1, Die Wu1, Ting Yang2
1Department of Breast and Thyroid Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
Cancers
|December 30, 2025
Summary
Connexin43 (Cx43) drives triple-negative breast cancer (TNBC) progression by regulating Rab31 and autophagy. Targeting Cx43 offers a potential therapeutic strategy for TNBC, improving treatment outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Connexin43 (Cx43) is a transmembrane protein with an unclear role in triple-negative breast cancer (TNBC).
- Understanding Cx43's expression and mechanisms is crucial for developing effective TNBC therapies.
Purpose of the Study:
- To investigate the expression profile and molecular mechanisms of Cx43 in TNBC.
- To elucidate the role of the Cx43/Rab31 axis in regulating autophagy and TNBC progression.
- To evaluate Cx43 as a potential therapeutic target for TNBC.
Main Methods:
- Systematic analysis of Cx43 expression in breast cancer cell lines and tissues.
- Functional assays (proliferation, migration, invasion) to assess Cx43's impact on TNBC progression.
- Identification and analysis of Cx43-interacting protein Rab31 and autophagy-related proteins.
- In vivo validation using a nude mouse model.
Main Results:
- Cx43 was upregulated in TNBC tissues and cell lines, enhancing proliferation, migration, and invasion.
- Cx43 co-expressed with Rab31, regulating its levels and modulating autophagy.
- Cx43 promoted tumor growth in vivo by affecting the Rab31/autophagy pathway.
Conclusions:
- The Cx43/Rab31 axis promotes TNBC progression through autophagy.
- Cx43 represents a promising therapeutic target for triple-negative breast cancer.
- Findings provide mechanistic insights for improving TNBC treatment strategies.
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