FDX1 enhances endometriosis cell cuproptosis via G6PD-mediated redox homeostasis.
Apoptosis
; 28(7-8): 1128-1140, 2023 08.
Article
in En
| MEDLINE
| ID: mdl-37119432
Cuproptosis is a new form of programmed cell death, which is associated with the mitochondrial TCA (tricarboxylic acid) cycle. But the functions of cuproptosis in endometriosis progression are still unknown. Here, we find that cuproptosis suppresses the growth of endometriosis cells and the growth of ectopic endometrial tissues in a mouse model. FDX1 as a key regulator in cuproptosis pathway could promote cuproptosis in endometriosis cells. Interestingly, FDX1 interacts with G6PD, and reduces its protein stability, which predominantly affects the cellular redox-regulating systems. Then, the reduced G6PD activity enhances cuproptosis via down-regulating NADPH and GSH levels. Collectively, our study demonstrates that FDX1 mediates cuproptosis in endometriosis via G6PD pathway, resulting in repression of endometriosis cell proliferation and metastasis.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Endometriosis
Limits:
Animals
Language:
En
Journal:
Apoptosis
Year:
2023
Document type:
Article
Country of publication:
Países Bajos