Ovarian tumorB1-mediated heat shock transcription factor 1 deubiquitination is critical for glycolysis and development of endometriosis

Xi Ling; Jiayi Lu; Xiaoyun Wang; Lan Liu; Lu Liu; Yadi Wang; Yujun Sun; Chune Ren; Chao Lu; Zhenhai Yu

doi:10.1016/j.isci.2022.105363

Ovarian tumorB1-mediated heat shock transcription factor 1 deubiquitination is critical for glycolysis and development of endometriosis

iScience. 2022 Oct 14;25(11):105363. doi: 10.1016/j.isci.2022.105363. eCollection 2022 Nov 18.

Authors

Xi Ling^{1

2}, Jiayi Lu^{1

2}, Xiaoyun Wang^{1

2}, Lan Liu^{1

2}, Lu Liu^{1

2}, Yadi Wang^{1

2}, Yujun Sun^{1

2}, Chune Ren¹, Chao Lu¹, Zhenhai Yu¹

Affiliations

¹ Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang 261000, China.
² School of Clinical Medicine, Weifang Medical University, Weifang 261000, China.

Abstract

Endometriosis is a common chronic condition characterized by abnormal growth of the endometrium outside the uterus. Heat shock transcription factor 1 (HSF1) is a significant regulator of the proteotoxic stress response and plays an essential role in developing endometriosis. However, the mechanisms regulating HSF1 protein stability in endometriosis remain unclear. Here, we demonstrate that OTUB1 interacts with HSF1 and promotes HSF1 protein stability through deubiquitination. In addition, OTUB1 enhances glycolysis and epithelial-mesenchymal transition of endometriosis cells, leading to promote proliferation, migration, and invasion of endometriosis cells. The progression of endometriosis is inhibited in an OTUB1-knockout mouse model. In summary, OTUB1 promotes the development of endometriosis by up-regulating HSF1. OTUB1/HSF1 axis may become a new therapeutic target for endometriosis.

Keywords: Molecular physiology; molecular biology.