Human MutY homolog induces apoptosis in etoposide‑treated HEK293 cells

Hahm,Soo‑Hyun; Chung,Ji  Hyung; Agustina,Lia; Han,Se‑Hee; Yoon,In‑Soo; Park,Jong‑Hwa; Kang,Lin‑Woo; Park,Jin  Woo; Na,Jong  Joo; Han,Ye  Sun

doi:10.3892/ol.2012.921

Human MutY homolog induces apoptosis in etoposide‑treated HEK293 cells

Authors:
- Soo‑Hyun Hahm
- Ji Hyung Chung
- Lia Agustina
- Se‑Hee Han
- In‑Soo Yoon
- Jong‑Hwa Park
- Lin‑Woo Kang
- Jin Woo Park
- Jong Joo Na
- Ye Sun Han
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Affiliations: Department of Advanced Technology Fusion, Konkuk University, Gwangjin‑gu, Seoul 143‑701, Republic of Korea, Yonsei Integrative Research Institute for Cerebral __AMB__ Cardiovascular Diseases (YIRIC), Yonsei University Health System, Seoul 120‑752, Republic of Korea, Department of Genetic Engineering and Graduate School of Biotechnology, Kyung Hee University, Yongin 446‑701, Republic of Korea, BioActs, DKC Corporation, Gojan‑dong, Namdong‑gu, Incheon 405‑820, Republic of Korea
Published online on: September 19, 2012 https://doi.org/10.3892/ol.2012.921
Pages: 1203-1208

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Abstract

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.

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