Assistant Professor,  Masonic Cancer Center ,

 Department of Laboratory Medicine and Pathology

University of Minnesota

主持人：朱卫国 教授（北京大学基础医学院生物化学与分子生物学系）

时　间：  2009年6月26日 (周五) AM 10：00

地　点：  生化楼308                                                

Increasing evidence suggests that forkhead transcription factor FOXO1 and transcription co-activator CBP function as tumor suppressors by modulating expression of genes that regulate cell proliferation, apoptosis, oxidative stress or DNA damage repair. Ongoing research in the Huang laboratory is aimed to understand how the potent functions of FOXO1 and CBP are tightly regulated by various post-translational mechanisms, such as phosphorylation, acetylation, and ubiquitination. Moreover, various approaches of biochemistry, molecular biology and genetics are being used in order to systematically assess the impact of dysregulation of these molecules on cell transformation and tumor formation in many organs, particularly in the prostate.

Publication list (selected)

1.       Gan, L., Liu, P., Lu, H., Chen, S., Yang, J., McCarthy, J.B., Knudsen, K.E., and Huang, H.* Cyclin D1 promotes anchorage-independent cell survival by inhibiting FOXO-mediated anoikis. Cell Death & Differentiation, in press.

2.       Liu, P., Li, S., Gan, L., Kao, T.P., and Huang, H.* A transcription-independent function of FOXO 1 in inhibition of androgen-independent activation of the androgen receptor in prostate cancer cells. Cancer Research 68: 10290-9, 2008.

3.       Liu, P., Kao, T.P., and Huang, H. * CDK1 promotes cell proliferation and survival via phosphorylation and inhibition of FOXO1 transcription factor. Oncogene 27: 4733-44, 2008.

4.       Huang, H., Regan, K.M., Lou, Z., Chen, J., and Tindall, D.J. CDK2-dependent phosphorylation of FOXO1 as an apoptotic response to DNA damage. Science 314: 294-297, 2006.

5.       Huang, H., Regan, K.M., Wang, F., Wang, D., Smith, D.I, van Deursen, J., and Tindall, D.J. Skp2 inhibits FOXO 1 in tumor suppression through ubiquitin-mediated degradation. Proc Natl Acad Sci U S A. 102(5): 1649-54, 2005.