Human MutY homolog induces apoptosis in etoposide-treated HEK293 cells
SOO‑HYUN HAHM ; JI HYUNG CHUNG ; YE SUN HAN ; JONG JOO NA ; JIN WOO PARK ; LIN‑WOO KANG ; JONG‑HWA PARK ; IN‑SOO YOON ; SE‑HEE HAN ; LIA AGUSTINA
Oncology Letters, Vol.4(6) : 1203~1208, 2012
Etoposide (ETP) treatment of ataxia telangiectasia mutated (ATM) and Rad3-related protein (ATR)-, topoisomerase-binding protein-1 (TopBP1) and human MutY homolog (hMYH)-depleted cells results in a significant reduction in apoptotic signaling. The association between ATR or TopBP1 and hMYH increased following ETP treatment. In hMYH knockdown cells, the interaction between ATR and TopBP1 decreased following ETP treatment. We suggest that hMYH functions as a sensor of ETP-induced apoptosis. The results suggest that in the absence of hMYH, cells are unable to recognize the damage signal and the ATR pathway is not activated.