Journal
GENES TO CELLS
Volume 18, Issue 3, Pages 195-202Publisher
WILEY-BLACKWELL
DOI: 10.1111/gtc.12027
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Funding
- Global COE Program 'Global Center for Education and Research in Integrative Membrane Biology'
- Targeted Proteins Research Program from the Ministry of Education, Culture, Sports, Science and Technology, Japan
- Japan Society for the Promotion of Science
- Core Research for Evolutional Science and Technology from the Japanese Science and Technology Agency
- Naito Foundation
- Sagawa Foundation
- Yasuda Medical Foundation
- Cell Science Research Foundation
- Grants-in-Aid for Scientific Research [24790284, 23130510, 23501268] Funding Source: KAKEN
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Necl-2/CADM1 is down-regulated by the promoter hypermethylation and/or the loss of heterozygosity at chromosome 11q23.2 in many types of cancers and serves as a tumor suppressor by interacting in cis with ErbB3 and suppressing the ligand-induced ErbB2/ErbB3 signaling for cell movement and death. However, the incidence of these epigenetic and genetic abnormalities of Necl-2 is 3060% in these cancers. We investigated here other mechanisms that down-regulate Necl-2. miR-214, that is frequently up-regulated in a variety of cancers, targeted the 3UTR of the Necl-2 mRNA directly, suppressed the translation of Necl-2 and enhanced the ligand-induced ErbB2/ErbB3 signaling in human colon cancer Caco-2 cells. Hypoxia reduced the Necl-2 protein level in a manner independent of miR-214 or hypoxia-inducible factor-1 in Caco-2 cells. These results indicate that miR-214 and hypoxia are novel regulators that down-regulate Necl-2 and enhance ErbB2/ErbB3 signaling.
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