Journal of International Obstetrics and Gynecology ›› 2025, Vol. 52 ›› Issue (3): 319-325.doi: 10.12280/gjfckx.20250173

• Research on Gynecological Malignancies: Review • Previous Articles     Next Articles

Research Progress on E3 Ubiquitin Ligases in the Cervical Cancer

LIAN Si-han, HAN Meng-fei, WANG Yu-jue, ZHAO Lin-yan, HU Yan()   

  1. Department of Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China (LIAN Si-han, WANG Yu-jue, ZHAO Lin-yan, HU Yan);Department of Ultrasound, Shaoxing People′s Hospital, Shaoxing 312000, Zhejiang Province, China (HAN Meng-fei)
  • Received:2025-02-24 Published:2025-06-15 Online:2025-06-19
  • Contact: HU Yan E-mail:Drhuyan@wmu.edu.cn

Abstract:

Cervical cancer is the common gynecological malignancy with a relatively high incidence and mortality rate, and it shows a trend of younger onset, seriously endangering women′s health. Persistent infection with high-risk human papilloma virus (HPV) is the key and initiating factor for the occurrence and development of cervical cancer. Although surgery, radiotherapy, and chemotherapy have greatly improved the prognosis of cervical cancer patients, the survival rate of advanced cervical cancer remains unsatisfactory. Therefore, finding targeted therapeutic targets can provide new methods for clinical diagnosis and treatment. As a key enzyme in the ubiquitination cascade reaction, E3 ubiquitin ligases is responsible for tagging ubiquitin molecules onto target proteins, thereby regulating their biological function. E3 ubiquitin ligases can be mainly divided into three major categories: RING-type, HECT-type, and RBR-type. They can block the persistent HPV infection state and inhibit the progression of cervical cancer through mechanisms such as regulating the proliferation of cervical cancer cells, participating in cell migration and invasion, affecting the cell cycle, regulating the sensitivity to radiotherapy and chemotherapy, and mediating immune evasion. In terms of application, using proteasome inhibitors or directly targeting E3 ubiquitin ligases can delay the progression of the disease. In recent years, newly developed proteolysis, targeting chimeras and molecular glues also show broad prospects in the field of treatment.

Key words: Ubiquitination, Ubiquitin-protein ligases, Uterine cervical neoplasms, Therapy, Human papilloma virus