Cancer Institute

  • Jian-Wei Gu

    Assistant Professor
    Molecular Cancer Therapeutics Program
    MD, 1982, Shanghai Medical College, Fudan University, Shanghai, China
    Postdoctoral Fellow, 1988-1995, Columbia University, New York, NY

    Contact information 
    2500 N State St, Room G162
    Jackson, MS 39216
    Phone: (601) 815-3402


    Research interests

    • Role of exercise in the adipose tissue accumulation and cancer progression
    • Mechanisms of alcohol in tumor angiogenesis and cancer progression: Role of oxidative stress
    • Interplay between VEGF and Notch signaling in tumor angiogenesis and cancer progression

    Research synopsis

    The research interests in my lab mainly focus on the metabolic control of angiogenesis and its role in cancer and cardiovascular disease. The growth and expansion of a tumor is mainly dependent on angiogenesis, the formation of new capillaries from pre-existing blood vessels. Vascular endothelial growth factor (VEGF) is the most critical regulator in angiogenesis and is commonly over-expressed in the most of tumors, in which tumor cells are under greater oxidative stress than normal cells. We have recently reported that VEGF and its receptors are the important biological markers for breast cancer malignancy and progression, and demonstrated that the paracrine effects (especially angiogenesis) and the autocrine effects (proliferation and migration) of VEGF are involved in promoting breast cancer progression. We also report that alcohol intake or obesity markedly increases tumor growth rate by mechanisms that involve up-regulation of VEGF pathways. Recent insights have shed light onto the interplay between VEGF and Notch signaling in angiogenesis. Clearly, inhibiting tumor angiogenesis can play a key role in cancer prevention and treatment. Our current research projects include: 1) postmenopausal obesity promotes tumor angiogenesis and breast cancer progression; 2) role of exercise-induced circulating angiostatic phenotype in the adipose tissue accumulation and breast cancer progression; 3) mechanisms of alcohol intake in tumor angiogenesis and breast cancer progression; 4) combination of EGCG (a green tea antioxidant) and SU11248 (a selective VEGF receptor inhibitor) to treat cancers including breast cancer; and 5) interplay between VEGF and Notch signaling in tumor angiogenesis and breast cancer progression.

    Recent accomplishments and honors

    • 2004 - Bronze Award for the Excellence in Research at the University of Mississippi Medical Center (2004).
    • 2004 - National Institutes of Health Explorative Research Grant Award, "Chronic Alcohol Consumption Induces Tumor Angiogenesis"
    • "Scientists led by Dr. Jian-Wei Gu at the University of Mississippi Medical Center show for the first time how alcohol may speed cancer progression"; "Drinking fuels growth of breast tumor"; "Exercise releases endostatin"; and "Green tea inhibits breast cancer in mice." These press releases were reported by more than 1,000 TV, radio stations, and other news agencies including Reuters News, BBC News, CBS News, ABC News, NBC News, Fox News, Newsweek and Reader's Digest.

    Selected publications

    • Young E et al. SU11248, a selective tyrosine kinases inhibitor suppresses breast tumor angiogenesis and growth via targeting both tumor vasculature and breast cancer cells. Cancer Biology & Therapy 10: 703-711, 2010
    • Brandon EL et al. Obesity promotes melanoma tumor growth: Role of leptin. Cancer Biology & Therapy 8: 1871-1879, 2009
    • Gu JW et al. Oral administration of pyrrolidine dithiocarbamate (PDTC) inhibits VEGF expression, tumor angiogenesis and growth of breast cancer in female mice. Cancer Biology & Therapy 8: 541-551, 2009
    • Gu JW et al. Long-term high salt diet causes hypertension and alters renal cytokine gene expression profiles in Sprague-Dawley rats. Journal of Peking University (Health Science) 41: 505-515, 2009
    • Gu JW et al. Vascular endothelial growth factor receptor inhibitor enhances dietary salt-induced hypertension in Sprague-Dawley (SD) rats. Am J Physiol Regul Integr Comp Physiol 297: R142-148, 2009