A type of fat, known as “white fat,” can fuel the growth of cancers in humans, especially when it’s found in excess. Previously, how this process occurred remain a mystery. Now, researchers from the University of Texas have discovered a switch that may control this obesity-induced cancer growth, giving hope for the development of new treatments.
Mikhail Kolonin, the senior author of the study, led a team that published their work in the journal Nature Communications.
“Some tumors rely on fat to grow aggressively,” said Kolonin. “We’ve discovered a molecular network without which fat no longer promotes tumor growth.”
The molecular switch they identified goes under the name of CXCL1--a chemokine that signals to cells to regulate their movement. When they blocked the expression of CXCL1 in a mouse model of obesity-induced prostate cancer, they were able to slow the cancer growth. They used prostate cancer as a model since it’s propagated and driven by the accumulation of white fat tissue.
Importantly, when they applied their findings to humans, they found CXCL1 elevated in the fat tissue of patients with prostate cancer and obesity, as compared to patient controls with prostate cancer and no obesity.
Deepening their findings, they overexpressed CXCL1 in a genetic mouse model and found that the switch signals to cells within the fat, called adipose stromal cells (ASCs), to move towards tumor tissue providing nutrients and support to the cancer.
With the potential for treating obese patients with cancer blocking the switch may hold therapeutic value for these patients. “We’re exploring multiple ASC-targeting strategies,” Kolonin said in a statement. “Blockade of CXCL1 function to recruit ASC to tumors could be developed to intervene in cancer progression.”
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