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Carboxyl-terminal modulator protein induces apoptosis by regulating mitochondrial function in lung cancer cells

Cited 7 time in Web of Science Cited 7 time in Scopus
Authors
Hwang, Soon-Kyung; Minai-Tehrani, Arash; Yu, Kyeong-Nam; Chang, Seung-Hee; Kim, Ji-Eun; Lee, Kee-Ho; Park, Jongsun; Beck, George R., Jr.; Cho, Myung-Haing
Issue Date
2012-05
Citation
International Journal of Oncology, Vol.40 No.5, pp.1515-1524
Keywords
CTMPapoptosismitochondrialung cancer cells
Abstract
Serine/threonine protein kinase 13 (PKB/Akt) is involved in cell survival and growth. Carboxyl-terminal modulator protein (CTMP), a novel Akt binding partner, prevents Akt activation at the plasma membrane in response to various stimuli, and thus possesses a tumor suppressor-like function. In a previous study, we have demonstrated that CTMP inhibits tumor progression by facilitating apoptosis in a mouse lung cancer model. However, the precise mechanism of CTMP-induced apoptosis remains to be elucidated. The present study was performed to examine the role of CTMP in mitochondrial-mediated apoptosis and regulation of mitochondrial function in human lung carcinoma cells. Our results showed that CTMP altered mitochondrial morphology and caused the release of cytochrome c by inhibiting OPA1 expression. Additionally, CTMP facilitated mitochondrial-mediated apoptosis by inhibiting heat-shock protein 27 and preventing cytochrome c interaction with Apaf-1. Our data suggest that CTMP may therefore play a critical role in mitochondrial-mediated apoptosis in lung cancer cells.
ISSN
1019-6439
URI
https://hdl.handle.net/10371/172399
DOI
https://doi.org/10.3892/ijo.2011.1319
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College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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