BMC Cancer BioMed Central Research article Open Access SSeCKS/Gravin/AKAP12 attenuates expression of proliferative and angiogenic genes during suppression of v-Src-induced oncogenesis Yongzhong Liu1, Lingqiu Gao2 and Irwin H Gelman*2 Address: 1Mucosal Immunology Unit, National Institutes of Health, Bethesda, MD 20892, USA and 2Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA Email: Yongzhong Liu -
[email protected]; Lingqiu Gao -
[email protected]; Irwin H Gelman* -
[email protected] * Corresponding author Published: 25 April 2006 Received: 24 January 2006 Accepted: 25 April 2006 BMC Cancer2006, 6:105 doi:10.1186/1471-2407-6-105 This article is available from: http://www.biomedcentral.com/1471-2407/6/105 © 2006Liu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: SSeCKS is a major protein kinase C substrate with kinase scaffolding and metastasis- suppressor activity whose expression is severely downregulated in Src- and Ras-transformed fibroblast and epithelial cells and in human prostate, breast, and gastric cancers. We previously used NIH3T3 cells with tetracycline-regulated SSeCKS expression plus a temperature-sensitive v-Src allele to show that SSeCKS re-expression inhibited parameters of v-Src-induced oncogenic growth without attenuating in vivo Src kinase activity. Methods: We use cDNA microarrays and semi-quantitative RT-PCR analysis to identify changes in gene expression correlating with i) SSeCKS expression in the absence of v-Src activity, ii) activation of v-Src activity alone, and iii) SSeCKS re-expression in the presence of active v-Src.