KyungWon Huh , PhD
Assistant Professor, PhD,
University of Colorado Health Sciences Center, 2001

Biography:
Dr. Huh received her B.S. in Biology from Ewha Women’s University, in Seoul, South Korea and obtained her M.S. in Biology from California State University, San Bernardino in 1992 and in Biomedical Science from the University of Colorado Health Sciences Center in 1995. She completed her Ph.D. in Microbiology and Immunology at the University of Colorado Health Sciences Center in 2001. She completed her postdoctoral fellowship at Harvard Medical School and Brigham and Womens Hospital, MA.

Research interests

Human Papilllomaviruses (HPVs) are small DNA viruses that specifically infect epithelial cells. So far approximately~200 different types of HPVs have been reported. Different types of HPVs cause benign and malignant diseases. Persistent infection with a subset of HPVs, especially HPV-16 and HPV-18, is highly associated with development of cervical cancer, which is one of the most common cancers in women in the world. Recent development of prophylactic vaccines against HPV is expected to decrease the incidents of cervical cancer over next decades. However vaccines may not be effective against pre- or already developed malignant lesions.

Aberrant integration of viral genomes into host genome leads to continuous expression of HPV E6 and E7 proteins. HPV E6 and E7 oncoproteins are small proteins that have no enzymatic activities but exhibit a variety of transforming activities in tissue culture cells. The expression of E6 and E7 proteins has also been shown to induce cervical cancer in a transgenic mouse model upon long-term treatment with estrogen.
The oncogenic activities of E6 and E7 proteins are believed to be mediated through interaction with different cellular proteins resulting in alteration of the cellular targets’ functions. It is well known that HPV E6 and E7 inactivate the p53 and the pRB tumor suppressors respectively.

We previously identified a number of additional HPV-16 E7 interacting cellular proteins using tandem affinity purification. We have shown that p600 is a cellular protein that is necessary for transformation function of HPV-16 E6 and E7. We have also demonstrated that the cullin 2 ubiquitin ligase complex is a novel cellular target that contributes to aberrant degradation of pRB tumor suppressor by HPV-16 E7.

Understanding the cancer-associated molecular roles and HPV mediated deregulation of novel cellular targets is a major focus in the laboratory.

Selected Publications

Waris G, Huh KW, Siddiqui A. Mitochondrially associated hepatitis B Virus X protein constitutively activates transcription factors STAT-3 and NFB via oxidative stress. Mol Cell Biol. 21, 7721-7730 (2001)

Rahmani Z*, Huh KW*, Lasher R, Siddiqui A. Hepatitis B virus X protein colocalizes to mitochondria with a human voltage-dependent anion channel, HVDAC3, and alters its transmembrane potential. J Virol. 74, 2840-2846 (2000) (*equal contribution)

Huh KW and Siddiqui A. Characterization of HBx association with mitochondria. Mitochondrio 1, 349-359 (2002)

Munger K, Baldwin A, Edwards KM, Hayakawa H,Nguyen CL, Owens M, Grace M, Huh KW. Mechanisms of human papilloma virus-induced oncogenesis, J.Virol. 78., 11451-11460 (2004)

Huh KW, DeMasi J, Ogawa H, Nakatani Y, Howley PM, Münger K. Association of the human papillomavirus type 16 E7 oncoprotein with the 600 kDa retinoblastoma protein associated factor, p600. Proc. Natl. Acad. Sci. USA 102, 11492-11497 (2005)

DeMasi J, Huh KW, Nakatani Y, Munger K, Howley PM. Bovine papillomavirus E7 transformation function correlates with cellular p600 protein binding. Proc. Natl. Acad. Sci. USA 102. 11486-11491 (2005)

Baldwin A, Huh KW, Munger K. The HPV E7 oncoprotein dysregulates steroid receptor coactivator-1 localization and function. J.Virol. 80, 6669-6677 (2006)

Huh KW, Zhou X, Hayakawa H, Cho JY, Libermann T.A., Jin J, Harper W. J., and Munger K. Human papillomavirus type 16 E7 oncoprotein associates with the cullin 2 ubiquitin ligase complex, which contributes to degradation of the retinoblastoma tumor suppressor. J. Virol. 81,9737-9747 (2007)