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YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway

Pikor, Larissa A., Lockwood, William W., Thu, Kelsie L., Vucic, Emily A., Chari, Raj, Gazdar, Adi F., Lam, Stephen, Lam, Wan L.·2013·Cancer Research
DOI 10.1158/0008-5472.can-13-1897PMC PMC3959870

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Abstract

Genetic analyses of lung cancer have helped found new treatments in this disease. We conducted an integrative analysis of gene expression and copy number in 261 non–small cell lung cancers (NSCLC) relative to matched normal tissues to define novel candidate oncogenes, identifying 12q13-15 and more specifically the YEATS4 gene as amplified and overexpressed in ∼20% of the NSCLC cases examined. Overexpression of YEATS4 abrogated senescence in human bronchial epithelial cells. Conversely, RNAi-mediated attenuation of YEATS4 in human lung cancer cells reduced their proliferation and tumor growth, impairing colony formation and inducing cellular senescence. These effects were associated with increased levels of p21WAF1 and p53 and cleavage of PARP, implicating YEATS4 as a negative regulator of the p21-p53 pathway. We also found that YEATS4 expression affected cellular responses to cisplastin, with increased levels associated with resistance and decreased levels with sensitivity. Taken together, our findings reveal YEATS4 as a candidate oncogene amplified in NSCLC, and a novel mechanism contributing to NSCLC pathogenesis. Cancer Res; 73(24); 7301–12. ©2013 AACR.

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Metadata

Authors
Pikor, L. A., Lockwood, W. W., Thu, K. L., Vucic, E. A., Chari, R., Gazdar, A. F., Lam, S., & Lam, W. L.
Affiliations
Authors' Affiliations: 1Integrative Oncology, BC Cancer Research Center, Vancouver, BC, Canada; 2National Institutes of Health, Bethesda, Maryland; 3Department of Genetics, Harvard Medical School, Boston, Massachusetts; and 4Hamon Center of Therapeutics, University of Texas South Western, Dallas, Texas
Venue
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2013-12-15
Volume
73
Issue
24
Pages
7301-7312
ISSN
  • 0008-5472
  • 1538-7445
DOI
10.1158/0008-5472.can-13-1897
PMC
PMC3959870
Cited by
44
References
2
Language
en

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