Xianglin Shi, Ph.D.
Professor

Graduate Center for Toxicology

Phone:
(859) 257-4054

Fax:
(859) 323-1059

E-mail:
xshi5@uky.edu

Dr. Shi’s laboratory focuses on investigation on molecular mechanism of metal-induced carcinogenesis. We are studying carcinogenic metal-induced generation of reactive oxygen species, oxidative stress, activations of transcription factors, gene expression, cell migration and invasion, actin filament reorganization, transformation, tumorigenesis, DNA damage and repair, cell cycle regulation, and apoptosis.  The long term goals are to provide a fundamental understanding concerning the mechanism of carcinogenic actions of metal compounds; to fill a need for the mechanistic information of cancer risk assessment for metal exposure; to propose methods for early detection; and to develop intervention and prevention strategies. The research interests of Dr. Shi’s laboratory also include mechanism-based disease prevention and control. We are studying the antioxidant properties of various naturally occurring antioxidants and to develop them as chemopreventive agents. The methods to be used include electron spin resonance (ESR) spectrometer and general molecular biology techniques.

Research Publications/Presentations:

Bower, J.J., Leonard, S.S., Chen, F., Shi, X. As(III) transcriptionally activates the gadd45a gene via the formation of H₂O₂. Free Radical Biology and Medicine 41, 285-294, 2006.

Ding, M., Feng, R., Wang, S.Y., Bowman, L., Lu, Y., Qian, Y., Castranova, V., Jiang, B.H., and Shi, X. Cyanidin-3-glucoside, a natural product derived from blackberry, exhibits chemopreventive and chemotherapeutic activity. Journal of Biological Chemistry 281, 17539-17368, 2006. 6.

Harris, G.K., Qian, Y., Leonard, S.S., Sbarra , D.C. , and Shi, X. Luteolin and chrysin differentially inhibit cyclooxygenase-2 expression and scavenge reactive oxygen species but similarly inhibit prostaglandin-E2 formation in RAW 264.7 cells. Journal of Nutrition 136, 1517-1521, 2006.

Bower, J.J., Leonard, S.S., and Shi, X. Molecular mechanisms of metal toxicity and carcinogenesis.  Molecular and Cellular Biochemistry 279, 3-15, 2005. 

Mohler, D.L., Downs , J.R., Hurley-Predecki, A.L., Sallman, J.R., Gannett, P.M., and Shi, X. DNA cleavage by the photolysis of cyclopentadienyl metal complexes: mechanistic studies and sequence selectivity of stress scission by CpW(CO)₃CH₃. Journal of Organic Chemistry 70, 9093-9102, 2005.

Bower, J.J., and Shi, X. Environmental health research in the post-genome era: new fields, new challenges, and new opportunities.  Journal of Toxicology and Environmental Health 8, 71-94, 2005.

Qian, Y., Liu, K.J., Chen, Y., Flynn , D.C. , Castranova, V., and Shi, X. Cdc42 regulates        arsenic-induced NADPH oxidase activation and cell migration through actin filament          reorganization. Journal of Biological Chemistry, 280, 3875-3884, 2005.

Leonard, S.S., Harris, G.K., and Shi, X. Metal-induced oxidative stress and signal transduction. Free Radical Biology and Medicine 37, 1921-1942, 2004.

Ding, M., Lu, Y., Bowman, L., Huang, H., Leonard, S., Wang, L., Vallyathan, V., Castranova, V., and Shi, X. Inhibition of AP-1 and neoplastic transformation by fresh apple peel extract. Journal of Biological Chemistry 279, 10670-10676, 2004.

Chen, F., Castranova, V., Li, Z., and Karin, M., and Shi, X. IKKbeta deficiency caused oxidative stress and prolonged JNK activation induced by arsenic. Cancer Research 63, 7689-7693, 2003. 

Qian, Y., Castranova, V., and Shi, X. New Perspectives in Arsenic-Induced Cell Signal Transduction. Journal of Inorganic Biochemistry 96, 271-278, 2003.

Qian, Y., Luo, J., Leonard, S.S., Harris, G.K., Millecchia, L., Flynn , D.C. , Shi, X. Hydrogen peroxide formation and actin filament reorganization by CDC42 are essential for ethanol-induced in vitro angiogenesis. Journal of Biological Chemistry 278, 16189-16197, 2003.

Zhang, Z., Leonard, S.S.., Huang, C., Vallyathan, V., Castranova, V., and Shi, X. Role of reactive oxygen species and MAPKs in vanadate induced G₂/M phase arrest.  Free Radical Biology and Medicine 34, 1333-1342, 2003.

Luo, J., Sun, Y., Lin, H., Qian, Y., Li, Z., Leonard, S.S., Huang, C., and Shi, X. Activation of JNK by vanadate induces a Fas-associated death domain (FADD)-dependent death of cerebellar granule progenitors in vitro.  Journal of Biological Chemistry 278, 4542-4551, 2003. 

Gao, N., Jiang, B., Leonard, S.S., Corum, L., Zhang, Z., Roberts, J.R., Antonini, J., Zheng, J.Z., Flynn, D.C., Castranova, V., and Shi, X. p38 signaling-mediated hypoxia-inducible factor 1a and vascular endothelial growth factor induced by Cr(VI) in DU145 human prostate carcinoma cells. Journal of Biological Chemistry 277, 45041-45048, 2002.

Gao, N., Ding, M., Zheng, J.Z., Zhang, Z., Leonard, S.S., Liu, K.J., Shi, X., and Jiang, B. Vanadate induced expression of hypoxia-inducible factor 1a and vascular endothelial growth factor through phosphatidylinositol 3-kinase/Akt pathway and reactive oxygen species. Journal of Biological Chemistry 277, 31963-31971, 2002.