Effect of Disrupting Seven-in-Absentia Homolog 2 Function on Lung Cancer Cell Growth | Zendy

Atique U. Ahmed | Zendy; Rebecca L. Schmidt | Zendy; Cheol Hong Park | Zendy; Nanette R. Reed | Zendy; Shayla Hesse | Zendy; Charles F. Thomas | Zendy; Julian R. Molina | Zendy; Claude Deschamps | Zendy; Ping Yang | Zendy; Marie Christine Aubry | Zendy; Amy Tang | Zendy

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Effect of Disrupting Seven-in-Absentia Homolog 2 Function on Lung Cancer Cell Growth

Author(s) -

Atique U. Ahmed,

Rebecca L. Schmidt,

Cheol Hong Park,

Nanette R. Reed,

Shayla Hesse,

Charles F. Thomas,

Julian R. Molina,

Claude Deschamps,

Ping Yang,

Marie Christine Aubry,

Amy Tang

Publication year - 2008

Publication title -

jnci journal of the national cancer institute

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.797

H-Index - 356

eISSN - 1460-2105

pISSN - 0027-8874

DOI - 10.1093/jnci/djn365

Subject(s) - carcinogenesis , epidermal growth factor receptor , signal transduction , lung cancer , cancer research , biology , ubiquitin , cell growth , ubiquitin ligase , microbiology and biotechnology , function (biology) , cancer , genetics , medicine , gene

Hyperactivated epidermal growth factor receptor (EGFR) and/or RAS signaling drives cellular transformation and tumorigenesis in human lung cancers, but agents that block activated EGFR and RAS signaling have not yet been demonstrated to substantially extend patients' lives. The human homolog of Drosophila seven-in-absentia--SIAH-1 and SIAH-2--are ubiquitin E3 ligases and conserved downstream components of the RAS pathway that are required for mammalian RAS signal transduction. We examined whether inhibiting SIAH-2 function blocks lung cancer growth.

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