Blocking the chemokine CXCL1 resulted in slowed growth of obesity-related prostate cancer in mice models.
Targeting the on and off switch for obesity-related prostate cancer may lead to an effective new treatment, according to a study published in Nature Communications.
"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 prostate cancer morbidity and mortality," the study authors wrote.
The switch researchers discovered is called chemokine CXCL1, which regulates cell trafficking. When blocked in mice models, the growth of obesity-related prostate cancer slowed.
In the study, researchers analyzed CXCL1 levels in tumor samples of patients with prostate cancer and obesity compared with prostate cancer patients who were not obese. Researchers found that CXCL1 signaling to adipose tissue was elevated in obese patients.
In excess fat, CXCL1 can recruit adipose stromal cells (ASC) fat cells to the tumor. These cells support blood-vessels that feed tumors.
"Some tumors rely on fat to grow aggressively," said senior study author Mikhail Kolonin, PhD. "We've discovered a molecular network without which fat no longer promotes tumor growth."
The researchers are studying an experimental drug in animal models that depletes ASC.
"We're exploring multiple ASC-targeting strategies," Dr Kolonin concluded. "Blockade of CXCL1 function to recruit ASC to tumors could be developed to intervene in cancer progression."