Signal Transduction Laboratory

Telephone: (518) 641-6428
Fax: (518) 641-6304
hlin@ordwayresearch.org

Research Focus

Dr. Lin and his Signal Transduction Laboratory team study molecular mechanisms of induction of apoptosis in cancer cells. Most of these mechanisms are p53-dependent and involve pharmacologic approaches to post-translational modifications of mutated, as well as wild-type, p53 or other transactivator proteins to promote programmed cell death. The post-translational modifications are dictated by signal transduction cascades. Human cancer cell models include prostate, breast, lung and head-and-neck tumors.

Other studies in the laboratory include membrane-initiated actions of non-peptide hormones, identification of membrane receptor proteins for non-peptide hormones and post-translational modifications of the superfamily of nuclear hormone receptors. The contribution of prostaglandins to tumorigenesis is also studied.

Selected Publications

www.pubmed.com

Zhang, S.L., Cao, J.H., Davis , F.B., Tang, H.Y., P.J. Davis and H.Y. Lin (2004) Estrogen inhibits resveratrol-induced posttranslational modification of p53 and apoptosis in breast cancer cells. British Journal of Cancer; 91: 178- 185.

Shih A., Zhang S.L., Cao, J.H., Boswell, S., Wu, Y-S, Tang, H.Y., Lennartz, M.R., Davis, F.B., P.J. Davis and H.Y. Lin (2004) Inhibitory effect of EGF on resveratrol-induced apoptosis in prostate cancer cells is mediated by protein kinase C-alpha. Molecular Cancer Therapeutics; 11: 1355-1364.

Parikh R.R., Gildener-Leapman N., Narendran A., Lin H.Y. , Lemanski N., Bennett J.A., Jacobson H.I. and Andersen T.T. (2005) Prevention of N-methyl-N-nitrosourea-induced breast cancer by alpha-fetoprotein (AFP)-derived peptide, a peptide derived from the active site of AFP. Clin Cancer Res. 11:8512-8520

Lin H.Y. , Lansing L., Merillon J-M, Davis, F.B., Tang, H.-Y., Shih A., Vitrac X, Krisa S., Keating T., Cao H.J., Bergh J.J., Quackenbush S. and P.J. Davis. (2006). Integrin alpha(V)beta3 contains a receptor site for resveratrol. FASEB J. In press.

Davis F.B., Tang H.Y., Shih A, Keating T., Lansing L., Hercgergs A, Fenstermarker RA, Mousa S, Mousa A, Davis P.J. and H.Y. Lin (2006). Acting via cell surface receptor, thyroid hormone is a growth factor for glioma cells. Cancer Research. In press.

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