Ho-Hyung Woo, PhD

Associate Scientist, Arizona Cancer Center

E-Mail Address: 
hwoo@AZCC.arizona.edu
Short Bio: 
Dr. Woo received his PhD from the University of Minnesota, Twin Cities, and his undergraduate degree from the Korea University, Seoul, Korea. He did postdoctoral work in the Memorial Sloan-Kettering Cancer Center, New York and also at the University of California, Los Angeles.
His research goal is to understand the molecular mechanisms of metastasis and perform translational research to develop therapeutic agents. He is interested particularly in how breast and ovarian cancer metastasize to other organs. His current research is focused on the molecular basis of metastasis in epithelial ovarian cancer and breast cancer. Abnormal expression of proto-oncogenes c-fms and/or CSF-1 is a critical factor in breast and epithelial ovarian cancer development. CSF-1 encodes macrophage colony stimulating factor (M-CSF) and c-fms encodes receptor tyrosine kinase, a sole receptor to CSF-1. Expression of c-fms and CSF-1 is regulated at both transcriptional and post-transcriptional levels.
 
Research Information
Summary of Research Activity: 
Translational Down-Regulation of Proto-Oncogene C-Fms by RNA-binding proteins in Breast Cancer
c-fms expression is regulated at both transcriptional and post-transcriptional level and 3’-UTR mRNA binding proteins are involved. Both HuR and vigilin proteins are working together to coordinate the proper level of expression of c-fms. Once this coordinated regulation by HuR and vigilin is dysregulated, c-fms expression increases and can cause breast cancer development.
 
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Antagonistic Effects between Glucocorticoids and Vigilin in Chromatin States of Proto-Oncogene C-Fms Locus in Breast Cancer
Half of human breast cancer tissue (52%) have functional glucocorticoids (GCs) receptors and is responsible for responsiveness to endogenous, circulating GCs. GCs were found to stimulate the invasive potential of some breast cancer cells (BT20, SKBR3) in vitro and also in experimental metastasis mouse model. Furthermore, GCs upregulate c-fms expression by up to 50-fold in breast cancer cells (BT20). In contrast vigilin downregulates c-fms transcription. we propose a model about epigenetic regulation of c-fms gene in breast cancer. In this model, glucocorticoids and vigilin have antagonistic effects for chromatin states in c-fms locus in breast cancer. Dysregulation of these two components could result breast cancer.
 
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Post-transcriptional Regulation of Macrophage Colony Stimulating Factor (CSF-1) in Ovarian Cancer
CSF-1 mRNA 3'UTR contains microRNA seed sequences, G-quadruplex element, and AU-rich elements (AREs). Comprehensive study of these cis-acting regulatory elements will give a clue to understand post-transcriptional and translational regulation of CSF-1 expression. Abnormal overexpression of CSF-1 is poor prognostic factor in ovarian cancer development.

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Selected Publications: 
1. Woo HH et al., (2012) miR-130a and miR-301a require RNA-binding protein nucleolin, not HuR, to repress CSF-1 mRNA in human ovarian cancer. In press.
2. Woo HH et al., (2012) Post-transcriptional regulation of proto-oncogene c-fms by RNA binding proteins in breast cancer. Oncogene Book chapter. In press.
3. Laszlo C., Woo HH et al., (2012) Post-transcriptional repression of macrophage colony stimulating factor by miR-128 and miR-152 in human ovarian cancer. In press.
4. Woo HH et al., (2011) Post-transcriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer. Molecular and Cellular Biology.
5. Toy EP, Woo HH et al., (2010) Inhibition of the c-fms proto-oncogene autocrine loop and tumor phenotype in glucocorticoid stimulated human breast carcinoma cells. Breast Cancer Research and Treatment.
6. Woo HH et al., (2009) Regulation of non-AU-rich element containing c-fms proto-oncogene expression by HuR in breast cancer. Oncogene.
Academic Information
Doctorate: 
University of Minnesota, Twin Cities
Undergraduate School: 
Korea University, Seoul, Korea