{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T14:50:48Z","timestamp":1785336648894,"version":"3.55.0"},"reference-count":25,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2011,4,1]],"date-time":"2011-04-01T00:00:00Z","timestamp":1301616000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2011,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The ability of SSeCKS\/Gravin\/AKAP12 (SSeCKS) to negatively regulate cell cycle progression is thought to relate to its spatiotemporal scaffolding activity for key signaling molecules such as protein kinase A and C, calmodulin and cyclins. SSeCKS is downregulated upon progression to malignancy in many cancer types, including melanoma and nonmelanoma skin cancer. The forced re\u2010expression of SSeCKS is especially potent in suppressing metastasis through the inhibition of VEGF\u2010mediated neovascularization. We have previously shown that SSeCKS\u2010null (KO) mice exhibit hyperplasia and focal dysplasia in the prostate marked by activated Akt. To address whether KO mice exhibit increased skin carcinogenesis, WT and KO C57BL\/6 mice were treated topically with 12\u2010<jats:italic>O<\/jats:italic>\u2010tetradecanoylphorbol\u201013\u2010acetate and 7,12\u2010dimethylbenzanthracene. Compared to WT mice, KO mice developed squamous papillomas more rapidly and in greater numbers and also exhibited significantly increased progression to squamous cell carcinoma. Untreated KO epidermal layers were thicker than those in age\u2010matched WT mice and exhibited significantly increased levels of FAK and phospho\u2010ERK1\/2, known mediators of carcinogen\u2010induced squamous papilloma progression to carcinoma. Compared to protein levels in WT mouse embryo fibroblasts (MEF), SSeCKS levels were increased in FAK\u2010null cells, whereas FAK levels were increased in SSeCKS\u2010null cells. RNAi studies in WT MEF cells suggest that SSeCKS and FAK attenuate each other's expression. Our study implicates a role for SSeCKS in preventing of skin cancer progression possibly through negatively regulating FAK expression.<\/jats:p>","DOI":"10.1002\/ijc.25828","type":"journal-article","created":{"date-parts":[[2010,12,2]],"date-time":"2010-12-02T14:54:16Z","timestamp":1291301656000},"page":"2025-2031","source":"Crossref","is-referenced-by-count":7,"title":["Carcinogen\u2010induced squamous papillomas and oncogenic progression in the absence of the SSeCKS\/AKAP12 metastasis suppressor correlate with FAK 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