Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 113, Issue 37, Pages E5481-E5490Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1610994113
Keywords
MYC; MYC-nick; colon cancer; motility; fascin
Categories
Funding
- [R01 CA20525]
- [R21 CA195126]
- [K99 CA190836]
- [T32CA080416]
- [14POST18230006]
- [2T32DK007742-16]
- [R01CA194663]
- [P30CA15704]
- [U01CA152756]
- [5R00CA151672]
- [CPRIT RR150059]
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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-beta, 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.
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