- Research Program: Carcinogenesis & Chemoprevention
- Hormel-Knowlton Professor
- McKnight Presidential Professor in Cancer Prevention
- Department of Cellular and Molecular Biology
- Executive Director, Hormel Institute
The major focus in the Cellular and Molecular Biology section is the molecular mechanisms of cancer development and the actions of chemopreventive agents in cancer prevention. The tumor promotion stage is a rate-limiting step in cancer development (carcinogenesis) and therefore understanding the molecular mechanisms in this step is important for progress toward cancer prevention.
We address response of mammalian cells to tumor promoters at the level of transcription factors and protein kinases. Our research examines the tumor promoter-induced signal transduction pathways and their role in the process of neoplastic cell transformation, carcinogenesis, and cancer prevention with the following:
- molecular and cell biological techniques
- transgenic mice
- mouse gene-knockout models
Another main emphasis of our lab is the elucidation of mechanism(s) of the anticancer actions attributed to several chemopreventive compounds. These are compounds considered to have little or no toxicity and are present in commonly consumed foods and beverages.
Zykova, T.A., Zhang, Y., Zhu, F., Bode, A.M., and Dong, Z. (2005) The signal transduction networks required for phosphorylation of STAT1 at Ser727 in mouse epidermal JB6 cells in the UVB response and inhibitory mechanisms of tea polyphenols. Carcinogenesis 26: 331-342.
He, Z., Cho, Y-Y, Ma, W-Y, Choi, H-S, Bode, A.M., and Dong, Z. (2005) Regulation of ultraviolet B-induced phosphorylation of histone H3 at serine 10 by Fyn kinase. J Biol Chem. 280: 2446-2454.
Dong, Z., Hoven, C.W., and Rosenfield, A. (2005) Lessons from the past. Nature 433: 573-574.
Ermakova, S., Choi, B-Y, Choi, H-S, Kang, B-S, Bode, A.M., and Dong, Z. (2005) The intermediate filament protein vimentin is a new target for EGCG. J Biol Chem. 280: 16882-16890.
Choi, H-S, Choi, B-Y, Cho, Y-Y, Zhu, F., Bode, A.M., and Dong, Z. (2005) Phosphorylation of ser28 in histone H3 mediated by mixed-lineage kinase-like mitogen-activated protein triple kinase alpha. J Biol Chem. 280: 13545-13553.
Cho, Y-Y, He, Z., Zhang, Y., Choi, H-S, Zhu, F., Choi, B-Y, Kang, B-S, Ma, W-Y, Bode, A.M., and Dong, Z. (2005) The p53 protein is a novel substrate of ribosomal S6 kinase 2 and a critical intermediary for ribosomal S6 kinase 2 and histone H3 interaction. Cancer Res. 65: 3596-3603.
Bode AM, Dong Z. Inducible covalent posttranslational modification of histone H3. Sci STKE 2005;2005:RE4.
Choi, B.Y., Choi, H.S., Ko, K., Cho, Y.Y., Zhu, F., Kang, B.S., Ermakova, S.P., Ma, W.Y., Bode, A.M. and Dong, Z. The tumor suppressor p16(INK4a) prevents cell transformation through inhibition of c-Jun phosphorylation and AP-1 activity. Nat Struct Mol Biol 12: 699-707, 2005
Choi, H.S., Choi, B.Y., Cho, Y.Y., Mizuno, H., Kang, B.S., Bode, A.M. and Dong, Z. Phosphorylation of histone H3 at serine 10 is indispensable for neoplastic cell transformation. Cancer Res 65: 5818-27, 2005
Ermakova, S., Choi, B.Y., Choi, H.S., Kang, B.S., Bode, A.M. and Dong, Z. The intermediate filament protein vimentin is a new target for epigallocatechin gallate. J Biol Chem 280: 16882-90, 2005
Lu, C., Zhu, F., Cho, Y.Y., Tang, F., Zykova, T., Ma, W.Y., Bode, A.M. and Dong, Z. Cell apoptosis: requirement of H2AX in DNA ladder formation, but not for the activation of caspase-3. Mol Cell 23: 121-32, 2006
Tatsumi, Y., Cho, Y.Y., He, Z., Mizuno, H., Seok Choi, H., Bode, A.M. and Dong, Z. Involvement of the paxillin pathway in JB6 Cl41 cell transformation. Cancer Res 66: 5968-74, 2006
Zhu, F., Choi, B.Y., Ma, W.Y., Zhao, Z., Zhang, Y., Cho, Y.Y., Choi, H.S., Imamoto, A., Bode, A.M. and Dong, Z. COOH-terminal Src kinase-mediated c-Jun phosphorylation promotes c-Jun degradation and inhibits cell transformation. Cancer Res 66: 5729-36, 2006