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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

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

  • Yi Huang1,2
  • Yidan Wang1,3
  • Ruiyun Li1,4
  • Yuan Yang1,2
4 affiliations
  1. 1The First Clinical Medical College, Lanzhou University, Lanzhou 730000, China
  2. 2The Reproductive Medicine Center, The First Hospital of Lanzhou University, Lanzhou 730000, China
  3. 3Base of Reproductive Medicine Transformation Application, Key Laboratory for Reproductive Medicine and Embryo, Gansu International Scientific and Technological Cooperation, Lanzhou 730000, China
  4. 4Department of Obstetrics and Gynecology, The First Hospital of Lanzhou University, Lanzhou 730000, China
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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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Cite

BibTeXRIS
BibTeX
@article{huang2026crmp4mediated,
  title = {{CRMP4-Mediated Regulation of Cav1.3 Protein Stability and Apoptosis Resistance in Endometriosis}},
  author = {Yi Huang and Yidan Wang and Ruiyun Li and Yuan Yang},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209291},
  url = {https://www.mdpi.com/1422-0067/27/20/9291},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - CRMP4-Mediated Regulation of Cav1.3 Protein Stability and Apoptosis Resistance in Endometriosis
AU  - Yi Huang
AU  - Yidan Wang
AU  - Ruiyun Li
AU  - Yuan Yang
PY  - 2026
DA  - 2026/10/19
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209291
UR  - https://www.mdpi.com/1422-0067/27/20/9291
AB  - 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.
SN  - 1422-0067
ER  -