Your browser doesn't support javascript.
loading
FXN targeting induces cell death in ovarian cancer stem-like cells through PRDX3-Mediated oxidative stress.
Xu, Shanshan; Liu, Yuwan; Yang, Shizhou; Fei, Weidong; Qin, Jiale; Lu, Weiguo; Xu, Junfen.
Affiliation
  • Xu S; Department of Gynecologic Oncology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, Zhejiang, China.
  • Liu Y; Women's Reproductive Health Laboratory of Zhejiang Province, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, Zhejiang, China.
  • Yang S; Department of Gynecologic Oncology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, Zhejiang, China.
  • Fei W; Department of Pharmacy, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, Zhejiang, China.
  • Qin J; Department of Ultrasound, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, Zhejiang, China.
  • Lu W; Department of Gynecologic Oncology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, Zhejiang, China.
  • Xu J; Zhejiang Provincial Clinical Research Center for Obstetrics and Gynecology, Hangzhou 310006, Zhejiang, China.
iScience ; 27(8): 110506, 2024 Aug 16.
Article in En | MEDLINE | ID: mdl-39184439
ABSTRACT
Ovarian cancer stem cells (OCSCs) significantly impact the prognosis, chemoresistance, and treatment outcomes in OC. While ferroptosis has been proven effective against OCSCs, the intricate relationship between ferroptosis and OCSCs remains incompletely understood. Here, we enriched ovarian cancer stem-like cells (OCSLCs) through mammosphere culture, as an OCSC model. OCSLCs displayed heightened ferroptosis susceptibility, correlating with elevated FXN levels compared to non-stem OC cells. FXN has recently emerged as a potential regulator in ferroptosis. FXN knockdown diminished stemness marker nanog, sphere-forming ability, increased reactive oxygen species (ROS) generation, and attenuated OCSLCs viability. FXN overexpression exacerbated ferroptosis resistance and reduced RSL3-induced cell death. FXN knockdown impeded OCSLC xenograft tumor growth and exacerbated the degeneration of peroxiredoxin 3 (PRDX3), a mitochondrial antioxidant protein participates in oxidative stress. Thus, elevated FXN in OCSLCs suppresses ROS accumulation, fostering ferroptosis resistance, and regulates the antioxidant protein PRDX3. FXN emerges as a potential therapeutic target for OC.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: IScience Year: 2024 Document type: Article Affiliation country: China Country of publication: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: IScience Year: 2024 Document type: Article Affiliation country: China Country of publication: United States