CRMP4-Mediated Regulation of Cav1.3 Protein Stability and Apoptosis Resistance in Endometriosis

Yi Huang, Yidan Wang, Ruiyun Li, Yuan Yang
In: International Journal of Molecular Sciences · 2026 · vol. 27(20) , pp. 9291 · doi:10.3390/ijms27209291 · W7222933481
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The study demonstrates that ZNF460-induced CRMP4 stabilizes Cav1.3 by inhibiting RNF138-mediated ubiquitination, thereby promoting apoptosis resistance in endometriosis cells and suggesting this axis as a therapeutic target.

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Abstract

Endometriosis (EMs) is a common chronic gynecological disorder characterized by the ectopic implantation and growth of endometrial-like tissue. The abnormal survival of ectopic endometrial cells, including their reduced susceptibility to apoptosis, plays an important role in the development of EMs. Cav1.3 is aberrantly upregulated in EMs and contributes to disease progression; however, the mechanism responsible for its increased expression remains unclear. In this study, protein stability and ubiquitination assays were performed in hEM15A cells. Cav1.3-interacting proteins were screened by co-immunoprecipitation coupled with liquid chromatography tandem mass spectrometry, and the regulatory pathway was further examined using in vitro experiments and animal models. We found that reduced ubiquitin–proteasome-mediated degradation increased Cav1.3 stability in hEM15A cells. Our results further showed that ZNF460 increased CRMP4 expression by activating its transcription. CRMP4 associated with Cav1.3 and reduced RNF138–Cav1.3 association, accompanied by decreased Cav1.3 ubiquitination and increased protein stability. ZNF460-dependent CRMP4 expression promoted Cav1.3 accumulation and was associated with reduced apoptosis in hEM15A cells. These findings clarify the post-translational mechanism underlying Cav1.3 upregulation in EMs and suggest that the ZNF460/CRMP4/RNF138/Cav1.3 axis may serve as a potential molecular target for EMs treatment.

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