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The sequestosome 1 protein: therapeutic vulnerabilities in ovarian cancer
Nurzadeh, Maryam; Ghalandarpoor-Attar, Seyedeh Mojgan; Rabiei, Maryam.
Affiliation
  • Nurzadeh, Maryam; Tehran University of Medical Sciences. Shariati Hospital. Fetomaternal Department. Tehran. Iran
  • Ghalandarpoor-Attar, Seyedeh Mojgan; Tehran University of Medical Sciences. Baharloo Hospital. Obstetrics and Gynecology Department. Tehran. Iran
  • Rabiei, Maryam; Tehran University of Medical Sciences. Obstetrics and Gynecology Department. Tehran. Iran
Clin. transl. oncol. (Print) ; 25(10): 2783-2792, oct. 2023. ilus
Article in En | IBECS | ID: ibc-225059
Responsible library: ES1.1
Localization: ES15.1 - BNCS
ABSTRACT
Ovarian cancer (OC) is the most deadly tumor that may develop in a woman's reproductive system. It is also one of the most common causes of death among those who have been diagnosed with cancer in women. An adapter protein known as sequestosome 1(SQSTM1) or p62 is primarily responsible for the transportation, degradation, and destruction of a wide variety of proteins. This adapter protein works in conjunction with the autophagy process as well as the ubiquitin proteasome degradation pathway. In addition, the ability of SQSTM1 to interact with multiple binding partners link SQSTM1 to various pathways in the context of antioxidant defense system and inflammation. In this review, we outline the processes underlying the control that SQSTM1 has on these pathways and how their dysregulation contributes to the development of OC. At the final, the therapeutic approaches based on SQSTM1 targeting have been discussed (AU)
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Collection: 06-national / ES Database: IBECS Main subject: Ovarian Neoplasms / Adaptor Proteins, Signal Transducing / Sequestosome-1 Protein Limits: Female / Humans Language: En Journal: Clin. transl. oncol. (Print) Year: 2023 Document type: Article
Search on Google
Collection: 06-national / ES Database: IBECS Main subject: Ovarian Neoplasms / Adaptor Proteins, Signal Transducing / Sequestosome-1 Protein Limits: Female / Humans Language: En Journal: Clin. transl. oncol. (Print) Year: 2023 Document type: Article