21 Jun Fat Cells Signal Cancer to Become More Aggressive

MedicalResearch.com Interview with:

Dr. Mikhail Kolonin

Mikhail Kolonin, PhD, Associate Professor
Director, Center for Metabolic and Degenerative Diseases
Harry E. Bovay, Jr. Distinguished University Chair in Metabolic Disease Research
The Brown Foundation Institute of Molecular Medicine
University of Texas Health Science Center at Houston
Houston, TX 77030

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Epidemiology studies have indicated that in obese patients progression of prostate, breast, colorectal, and other cancers is more aggressive. Adipose (fat) tissue, expanding and undergoing inflammation in obesity, directly fuels tumor growth. Adipose tissue is composed by adipocytes and stromal/vascular cells, which secrete tumor-trophic factors. Previous studies by our group have demonstrated that adipose stromal cells, which support blood vessels and serve as adipocyte progenitors, are recruited by tumors and contribute to cancer progression. Mechanisms underlying stromal cell trafficking from fat tissue to tumors have remained obscure. We discovered that in obesity a chemokine CXCL1, expressed by cancer cells, attracts adipose stromal cells to tumors.

MedicalResearch.com: What should readers take away from your report?

Response: As the prevalence of obesity is rising, insights into the mechanisms underlying its link with cancer aggressiveness are urgently needed to develop new strategies for reducing cancer morbidity and mortality. In our study, CXCL1 signaling was found to be higher in the obese patients with prostate cancer. Blockade of CXCL1, or of its receptor on adipose stroma slowed the obesity-induced progression of prostate cancer in mouse models. This reveals a molecular switch, turned on in obesity, that activates cell trafficking to tumor.

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: Mechanisms responsible for CXCL1 expression activation in cancer cells need to be investigated. Blockade of CXCL1 function to recruit adipose stromal cells to tumors could be developed to intervene in cancer progression. That could be achieved by inhibiting CXCL1 or its receptor on stromal cells.

MedicalResearch.com: Is there anything else you would like to add?

Response: Recently, our group has also reported an approach to depletion of adipose stromal cells. Experimental compounds targeting adipose stroma prevented diet-induced obesity and tumor growth in mouse models. Future studies will establish if this approach can complement approved anti-obesity and anti-cancer treatments.

MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.

Citation:

1. Tao Zhang, Chieh Tseng, Yan Zhang, Olga Sirin, Paul G. Corn, Elsa M. Li-Ning-Tapia, Patricia Troncoso, John Davis, Curtis Pettaway, John Ward, Marsha L. Frazier, Christopher Logothetis, Mikhail G. Kolonin. CXCL1 mediates obesity-associated adipose stromal cell trafficking and function in the tumour microenvironment. Nature Communications, 2016; 7: 11674 DOI: 10.1038/ncomms11674

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Last Updated on June 21, 2016 by Marie Benz MD FAAD