Cancer type | Biomolecular mechanism | References |
---|---|---|
Prostate cancer | HDECR1 silencing induced ferroptosis by accumulation of PUFAs and then promoting ROS generation | [38] |
Silencing of PANX2 promoted ferroptosis by suppressing the expression of Nrf2 | [41] | |
PI3K/AKT/mTOR inhibited ferroptosis via upregulating SREBP1/SCD1 | [50] | |
HSPB1inhibited ferroptosis by promoting iron uptake and increasing lipid ROS production | [65] | |
Bicalutamide-iron combination induced ferroptosis | [28] | |
The combination of erastin and docetaxel induced ferroptosis | [111] | |
CHAC1 inhibits cell viability and increases the sensitivity of prostate cancer cells to docetaxel by inducing ferroptosis | [67] | |
Therapy-induced lipid uptake and remodeling underpin GPX4 dependence and ferroptosis hypersensitivity | [70] | |
Kidney cancer | VHL/HIF-2α induced ferroptosis via elevating lipid peroxidation levels through HILPDA | [73] |
TAZ silencing reduce sensitivity to erastin-induced ferroptosis by downregulating the expression of EMP1-NOX4 | [79] | |
ACOT8 inhibited ferroptosis | [86] | |
Repression of SUV39H1 induced ferroptosis via enhancing DPP4 activity | [89] | |
The low-expression of NCOA4 conferred ccRCC cells resistance to ferroptosis by increasing FTH and FTMT expression levels | [96] | |
GPX1 induced ferroptosis in KIPP | [101] | |
ART induced ferroptosis and enhanced the anti-tumor effect of sunitinib | ||
Bladder cancer | CPNPs targeted to EDNRB via EDN3-CPNPs and thereby induced ferroptosis | [121] |
Quinazolinyl-arylurea derivatives induced ferroptosis through ROS generation and GSH depletion | [122] |