| Literature DB >> 27566402 |
Sarah Anderson1, Kumud Raj Poudel1, Minna Roh-Johnson1, Thomas Brabletz2, Ming Yu3, Nofit Borenstein-Auerbach4, William N Grady5, Jihong Bai1, Cecilia B Moens1, Robert N Eisenman6, Maralice Conacci-Sorrell7.
Abstract
MYC-nick is a cytoplasmic, transcriptionally inactive member of the MYC oncoprotein family, generated by a proteolytic cleavage of full-length MYC. MYC-nick promotes migration and survival of cells in response to chemotherapeutic agents or withdrawal of glucose. Here we report that MYC-nick is abundant in colonic and intestinal tumors derived from mouse models with mutations in the Wnt, TGF-β, and PI3K pathways. Moreover, MYC-nick is elevated in colon cancer cells deleted for FBWX7, which encodes the major E3 ligase of full-length MYC frequently mutated in colorectal cancers. MYC-nick promotes the migration of colon cancer cells assayed in 3D cultures or grown as xenografts in a zebrafish metastasis model. MYC-nick accelerates migration by activating the Rho GTPase Cdc42 and inducing fascin expression. MYC-nick, fascin, and Cdc42 are frequently up-regulated in cells present at the invasive front of human colorectal tumors, suggesting a coordinated role for these proteins in tumor migration.Entities:
Keywords: MYC; MYC-nick; colon cancer; fascin; motility
Mesh：
Substances：
Year: 2016 PMID： 27566402 PMCID： PMC5027433 DOI： 10.1073/pnas.1610994113
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205