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Regulation of C-X-C chemokine gene expression by keratin 17 and hnRNP K in skin tumor keratinocytes.

Abstract
High levels of the intermediate filament keratin 17 (K17) correlate with a poor prognosis for several types of epithelial tumors. However, the causal relationship and underlying mechanisms remain undefined. A recent study suggested that K17 promotes skin tumorigenesis by fostering a specific type of inflammation. We report here that K17 interacts with the RNA-binding protein hnRNP K, which has also been implicated in cancer. K17 is required for the cytoplasmic localization of hnRNP K and for its role in regulating the expression of multiple pro-inflammatory mRNAs. Among these are the CXCR3 ligands CXCL9, CXCL10, and CXCL11, which together form a signaling axis with an established role in tumorigenesis. The K17-hnRNP K partnership is regulated by the ser/thr kinase RSK and required for CXCR3-dependent tumor cell growth and invasion. These findings functionally integrate K17, hnRNP K, and gene expression along with RSK and CXCR3 signaling in a keratinocyte-autonomous axis and provide a potential basis for their implication in tumorigenesis.
AuthorsByung Min Chung, Artem Arutyunov, Erika Ilagan, Nu Yao, Marsha Wills-Karp, Pierre A Coulombe
JournalThe Journal of cell biology (J Cell Biol) Vol. 208 Issue 5 Pg. 613-27 (Mar 02 2015) ISSN: 1540-8140 [Electronic] United States
PMID25713416 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Copyright© 2015 Chung et al.
Chemical References
  • CXCR3 protein, human
  • Chemokines, CXC
  • Cxcr3 protein, mouse
  • Heterogeneous-Nuclear Ribonucleoprotein K
  • Krt17 protein, mouse
  • Neoplasm Proteins
  • Receptors, CXCR3
  • Keratins
Topics
  • Animals
  • Chemokines, CXC (biosynthesis, genetics)
  • Gene Expression Regulation, Neoplastic
  • HeLa Cells
  • Heterogeneous-Nuclear Ribonucleoprotein K (genetics, metabolism)
  • Humans
  • Keratinocytes (metabolism)
  • Keratins (genetics, metabolism)
  • Mice, Knockout
  • Neoplasm Proteins (genetics, metabolism)
  • Receptors, CXCR3 (genetics, metabolism)
  • Signal Transduction (genetics)
  • Skin Neoplasms (genetics, metabolism, pathology)

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