NDLI: Mieap suppresses murine intestinal tumor via its mitochondrial quality control

Content Provider	PubMed Central
Author	Tsuneki, Masayuki Nakamura, Yasuyuki Kinjo, Takao Nakanishi, Ruri Arakawa, Hirofumi
Copyright Year	2015
Abstract	Mieap, a novel p53-inducible protein, plays a key role in maintaining healthy mitochondria in various pathophysiological states. Here, we show that Mieap deficiency in ApcMin/+ mice is strikingly associated with the malignant progression of murine intestinal tumors. To understand the role that Mieap plays in in vivo tumorigenesis, we generated Mieap heterozygous (ApcMin/+ Mieap+/−) and homozygous (ApcMin/+ Mieap−/−) ApcMin/+ mice. Interestingly, the ApcMin/+ mice with the Mieap+/− and Mieap−/− genetic background revealed remarkable shortening of the lifetime compared to ApcMin/+ mice because of severe anemia. A substantial increase in the number and size of intestinal polyps was associated with Mieap gene deficiency. Histopathologically, intestinal tumors in the Mieap-deficient ApcMin/+ mice clearly demonstrated advanced grades of adenomas and adenocarcinomas. We demonstrated that the significant increase in morphologically unhealthy mitochondria and trace accumulations of reactive oxygen species may be mechanisms underlying the increased malignant progression of the intestinal tumors of Mieap-deficient ApcMin/+ mice. These findings suggest that the Mieap-regulated mitochondrial quality control plays a critical role in preventing mouse intestinal tumorigenesis.
Related Links	http://dx.doi.org/10.1038/srep12472
Starting Page	12472
File Format	PDF
ISSN	20452322
e-ISSN	20452322
Journal	Scientific Reports
Volume Number	5
Language	English
Publisher	Nature Publishing Group
Publisher Date	2015-07-28
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Science and technology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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