NDLI: Mieap-regulated mitochondrial quality control is frequently inactivated in human colorectal cancer

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Mieap-regulated mitochondrial quality control is frequently inactivated in human colorectal cancer

Content Provider	PubMed Central
Author	Kamino, H. Nakamura, Y. Tsuneki, M. Sano, H. Miyamoto, Y. Kitamura, N. Futamura, M. Kanai, Y. Taniguchi, H. Shida, D. Kanemitsu, Y. Moriya, Y. Yoshida, K. Arakawa, H.
Copyright Year	2016
Abstract	Mieap, a p53-inducible protein, controls mitochondrial quality by repairing or eliminating unhealthy mitochondria. BNIP3 and NIX are critical mediators for the Mieap-regulated mitochondrial quality control. Mieap suppresses murine intestinal tumor via its mitochondrial quality control function. To explore the role of the Mieap-regulated mitochondria quality control function in colorectal cancer patients, we examined the statuses of p53, Mieap, BNIP3 and NIX in 57 primary colorectal cancer tissues. Promoter methylation of the Mieap and BNIP3 genes was found in 9% and 47% of colorectal cancer cases, respectively, whereas p53 mutation was found in more than 50% of colorectal cancer tissues lacking methylation of the Mieap and BNIP3 promoters, implying that the p53/Mieap/BNIP3-regulated mitochondria quality control pathway is inactivated in more than 70% of colorectal cancer patients. In LS174T colorectal cancer cells, hypoxia activated the Mieap-regulated mitochondria quality control function. Knockdown of p53, Mieap or BNIP3 in LS174T cells severely impaired the hypoxia-activated function, leading to the accumulation of unhealthy mitochondria and increase of mitochondrial reactive oxygen species generation. The mitochondrial reactive oxygen species generated by unhealthy mitochondria in the p53/Mieap/BNIP3-deficient cells remarkably enhanced cancer cell migration and invasion under hypoxic condition. These results suggest that the Mieap-regulated mitochondria quality control has a critical role in colorectal cancer suppression in the in vivo hypoxic tumor microenvironment.
Related Links	http://dx.doi.org/10.1038/oncsis.2015.43
Starting Page	181
File Format	PDF
ISSN	21579024
e-ISSN	21579024
Journal	Oncogenesis
Issue Number	1
Volume Number	5
Language	English
Publisher	Nature Publishing Group
Publisher Date	2016-01-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Cancer Research

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