A Novel Role for Keratin 17 in Coordinating Oncogenic Transformation and Cellular Adhesion in Ewing Sarcoma | Zendy

Savita Sankar | Zendy; Jason M. Tanner | Zendy; Russell Bell | Zendy; Aashi Chaturvedi | Zendy; R. Lor Randall | Zendy; Mary C. Beckerle | Zendy; Stephen L. Lessnick | Zendy

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A Novel Role for Keratin 17 in Coordinating Oncogenic Transformation and Cellular Adhesion in Ewing Sarcoma

Author(s) -

Savita Sankar,

Jason M. Tanner,

Russell Bell,

Aashi Chaturvedi,

R. Lor Randall,

Mary C. Beckerle,

Stephen L. Lessnick

Publication year - 2013

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.00241-13

Subject(s) - biology , cancer research , protein kinase b , gli1 , oncogene , microbiology and biotechnology , transcription factor , signal transduction , gene , hedgehog signaling pathway , genetics , cell cycle

Oncogenic transformation in Ewing sarcoma is caused by EWS/FLI, an aberrant transcription factor fusion oncogene. Glioma-associated oncogene homolog 1 (GLI1) is a critical target gene activated by EWS/FLI, but the mechanism by which GLI1 contributes to the transformed phenotype of Ewing sarcoma was unknown. In this work, we identify keratin 17 (KRT17) as a direct downstream target gene upregulated by GLI1. We demonstrate that KRT17 regulates cellular adhesion by activating AKT/PKB (protein kinase B) signaling. In addition, KRT17 is necessary for oncogenic transformation in Ewing sarcoma and accounts for much of the GLI1-mediated transformation function but via a mechanism independent of AKT signaling. Taken together, our data reveal previously unknown molecular functions for a cytoplasmic intermediate filament protein, KRT17, in coordinating EWS/FLI- and GLI1-mediated oncogenic transformation and cellular adhesion in Ewing sarcoma.

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