The results of the present study identified a potentially novel therapeutic target for prostate cancer, which may be useful in patients with castration-resistant prostate cancer.ĬhaC glutathione specific γ-glutamylcyclotransferase 1 cell viability endoplasmic reticulum stress ferroptosis prostate cancer sensitivity to docetaxel.ĬHAC1 inhibits cell viability and reduces intracellular GSH levels in DU145 cells and 22RV1 cells. The cellular mechanism may involve the induction of ER stress and ferroptosis. In summary, CHAC1 may inhibit cell viability and increase the sensitivity of prostate cancer cells to DTX. This inhibition was also eliminated following the addition of a ferroptosis inhibitor. Following transfection with plasmid overexpressing CHAC1, ER markers, BIP and CHOP levels, were significantly upregulated (P0.05). The expression levels of several endoplasmic reticulum (ER) stress-related factors were then measured by western blot analysis. Compared with non-tumor human prostate epithelial RWPE-1 cells, the mRNA and protein levels of CHAC1 significantly decreased in two prostate cancer cell lines, DU145 and 22RV1, as measured by quantitative polymerase chain reaction and western blot analysis (P0.05). The present study aimed to determine the effects and mechanism of ChaC glutathione specific γ-glutamylcyclotransferase 1 (CHAC1) on cell viability and the sensitivity of prostate cancer cells to docetaxel.

Chac inspections