Abstract 904: The TNIK kinase is a potential target in non-small cell lung and gastric cancer

Abstract

Abstract Traf2- and Nck-interacting kinase (TNIK) is one of germinal centre kinase (GCK) family members involved in cytoskeleton organization and neuronal dendrite extension. Emerging evidence indicated that TNIK is essential in activation of WNT pathway and colon cancer growth. To search for novel genetic aberrations that drive carcinogenesis, we performed microarray-based comparative hybridization (aGCH) to screen gene copy number variations in primary tumor samples and found TNIK gene is amplified in 19.2 % (29/151) of Chinese non-small cell lung cancer and 7 % (8/106) of Chinese gastric cancer patients. Interestingly, the amplification in NSCLC is highly enriched in squamous NSCLC patients (41.1%, 28/68). Theses amplifications were confirmed by fluorescence in situ hybridization (FISH) analysis. To further understand the function of TNIK gene amplification, PAMC82 human gastric cancer and T47D colon cancer cell lines with TNIK amplification were identified. RNA-interference-mediated silencing of TNIK resulted in significantly reduced cell growth and increased cell death in the TNIK amplified, but not in the non-amplified, tested cell lines. Together, our results suggest that TNIK is a novel therapeutic target in NSCLC and gastric cancer and TNIK amplification can be potentially used for patient selection. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 904. doi:1538-7445.AM2012-904