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University of Colorado Cancer Center

University of Colorado Cancer Center, A National Cancer Institute-designated Comprehensive Cancer Center

Cheng-Jun Hu, PhD



Tumor progression, invasion and metastasis and Cellular and Tumor Microenvironment


Craniofacial Biology


UCD, Anschutz Medical Campus, Dept of Craniofacial Biology, Aurora 

Contact: (303) 724-4576


1 Year of College

Number of Openings: 2

Program Objective:

1. Investigate the roles of hypoxia-inducible factors (HIF1a and HIF2a) in tumor progression and metastasis. 2. Investigate the transcriptional cofactors that are required for transcriptional activity of HIF1a and HIF2a to block HIF transcriptional activity for solid tumor treatment. 

Program Description:

Hypoxic microenvironments are frequently found in solid tumors as a result of an imbalance between oxygen supply and consumption. Tumor hypoxia is a major therapeutic concern since it reduces the effectiveness of radiotherapy and oxygen-dependent cytotoxic agents. Tumor hypoxia is also a driving force for malignant progression by hypoxia-inducible factor (HIF)-mediated activation of angiogenesis, anaerobic metabolism, and other processes that enable tumor cells to survive or escape their oxygen-deficient environment. Since this pathway operates in almost all solid malignancies, understanding the function and regulation of HIF will have a broad impact on cancer biology.  Transcriptional responses to hypoxia are primarily mediated by hypoxia inducible factors (HIFs), HIF1a and HIF2a.  HIF1a and HIF2a exhibit extensive structural similarities, however, we and others have determined that HIF1a and HIF2a activate different target genes and require distinct transcriptional cofactors for their transcriptional activity.  We are currently deleting or over-expressing HIF1a and/or HIF2a in mouse strains that have head-and-neck cancers to investigate the roles of HIF in tumor progression and metastasis.  In addition, we are investigating the transcriptional cofactors that are required for transcriptional activity of HIF1a and HIF2a.  Understanding the interactions between HIF and its cofactors will lay down a foundation to specifically block HIF transcriptional activity for solid tumor treatment.