Please use this identifier to cite or link to this item: https://doi.org/10.1038/onc.2011.57
Title: Overexpression of TRIB2 in human lung cancers contributes to tumorigenesis through downregulation of C/EBPα
Authors: Grandinetti, K.B.
Stevens, T.A.
Ha, S.
Salamone, R.J.
Walker, J.R.
Zhang, J.
Agarwalla, S.
Tenen, D.G. 
Peters, E.C.
Reddy, V.A.
Keywords: C/EBPα
lung
tribbles
TRIM21n
Issue Date: 28-Jul-2011
Citation: Grandinetti, K.B., Stevens, T.A., Ha, S., Salamone, R.J., Walker, J.R., Zhang, J., Agarwalla, S., Tenen, D.G., Peters, E.C., Reddy, V.A. (2011-07-28). Overexpression of TRIB2 in human lung cancers contributes to tumorigenesis through downregulation of C/EBPα. Oncogene 30 (30) : 3328-3335. ScholarBank@NUS Repository. https://doi.org/10.1038/onc.2011.57
Abstract: Lung cancer is the most common cause of cancer-related mortality worldwide. Here, we report elevated expression of tribbles homolog 2 (TRIB2) in primary human lung tumors and in non-small cell lung cancer cells that express low levels of differentiation-inducing transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα). In approximately 10-20% of cases, elevated TRIB2 expression resulted from gene amplification. TRIB2 knockdown was found to inhibit cell proliferation and in vivo tumor growth. In addition, TRIB2 knockdown led to morphological changes similar to C/EBPα overexpression and correlated with increased expression and activity of C/EBPα. TRIB2-mediated regulation of C/EBPα was found to occur through the association of TRIB2 with the E3 ligase TRIM21. Together, these data identify TRIB2 as a potential driver of lung tumorigenesis through a mechanism that involves downregulation of C/EBPα. © 2011 Macmillan Publishers Limited All rights reserved.
Source Title: Oncogene
URI: http://scholarbank.nus.edu.sg/handle/10635/125429
ISSN: 09509232
DOI: 10.1038/onc.2011.57
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