Roles of ferroptosis in urologic malignancies

Cancer Cell International

Biao Qian¹  Weizhou Wu²  Peng Li³  Xin Li⁴  Maolei Shen⁴  Shankun Zhao⁴  Qinzhang Wang⁵ 

[1] Department of Urology, First Affiliated Hospital of Gannan Medical University, 341000, Ganzhou, Jiangxi, China;Department of Urology, Maoming People’s Hospital, 525000, Maoming, Guangdong, China;Department of Urology, Qingdao Women and Children’s Hospital, 266000, Qingdao, Shandong, China;Department of Urology, Taizhou Central Hospital (Taizhou University Hospital), 318000, Taizhou, Zhejiang, China;Department of Urology, The First Affiliated Hospital of Shihezi University Medical School, Shihezi, China;

关键词: Ferroptosis;    Regulated cell death;    Urologic oncology;    Mechanism;    Therapy;   

DOI  :  10.1186/s12935-021-02264-5

来源: Springer

【 摘 要 】

Ferroptosis, an iron-dependent form of non-apoptotic cell death, is believed to strongly contribute to the pathogenesis of multiple cancers. Recently, the positive association between ferroptosis and urologic malignancies has drawn considerable attention, while a comprehensive review focused on this issue is absent. Based on this review, ferroptosis has been implicated in the development and therapeutic responses of prostate cancer, kidney cancer, and bladder cancer. Mechanistically, a large number of biomolecules and tumor-associated signaling pathways, including DECR1, PANX2, HSPB1, ACOT8, SUV39H1, NCOA4, PI3K-AKT-mTOR signaling, VHL/HIF-2α pathway, and Hippo/TAZ signaling pathway, have been reported to regulate ferroptosis in urologic cancers. Ferroptosis inducers, such as erastin, ART, CPNPs, and quinazolinyl-arylurea derivatives, exert potential therapeutic effects per se and/or enhance the anticancer response of other anticancer drugs in urologic oncology. A better understanding of ferroptosis may provide a promising way to treat therapy-resistant urologic cancers.

【 授权许可】

CC BY