Study Reveals How Fat Cells Fuel Breast Cancer Growth
A new study published in Nature Communications offers insight into why obesity increases the risk of developing certain cancers, including breast cancer. Researchers found that tumor cells can directly communicate with nearby fat cells and use them as a fuel source for their own growth.
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They found that breast cancer cells form channels called gap junctions with adjacent fat cells called adipocytes. Through these channels, the tumor cells signal fat cells to release stored lipids. Those lipids are then consumed by the tumor to support growth and spread.
Tiffany Carson, PhD
“This study provides a potential mechanism by which excess adiposity, the defining feature of obesity, may drive cancer development and tumor growth in obesity-associated cancers such as breast cancer,” said Tiffany Carson, PhD, a researcher in the Department of Health Outcomes and Behavior at Moffitt Cancer Center. “We have known for many years that obesity is associated with increased risk for development of at least 13 different cancers. However, the mechanisms have not been fully elucidated, leading to limited opportunities for targeted interventions. In this study leveraging human patient samples and mouse models, this team has shown that fat cells in normal adjacent tissue can be used by tumors to fuel their own growth.”
A Conversation Between Tumor and Fat Cells
Carson explained that one of the most important findings is the evidence supporting contact-dependent signaling between fat and tumor cells.
“The tumor ‘tells’ the fat cells to release their lipids, which are then used by the tumor cells for growth,” she said. “This process, called lipolysis, is essentially the breakdown of fats and lipids to release fatty acids. The gap junctions serve as the communication channel that allows this to happen.”
Implications for Triple-Negative Breast Cancer
The research also focused on triple-negative breast cancer, an aggressive subtype that is more common and harder to treat in people with obesity.
“There are several reasons why triple-negative breast cancer is harder to treat in people with obesity including a weakened immune response, challenges in appropriate chemotherapy dosing and other comorbidities,” Carson said. “These findings may also add to the list of challenges in treating it in people with obesity. This research with a specific focus on triple-negative breast cancer highlights how adjacent fat cells fuel tumor growth, which may limit treatment success.”
Looking Ahead
While the study sheds light on how tumors exploit fat cells, it also raises new questions for scientists.
“This study provides key insight into a potential mechanism linking obesity and cancer, which is critical for our understanding of potential targeted interventions,” Carson said. “For example, can the path between the tumor cells and fat cells be blocked so that the tumor cells can no longer feed on the adjacent fat cells? Another key question in this area is whether shrinking fat cells through weight loss is beneficial for lowering cancer risk and improving outcomes, and if so, how much weight loss is needed.”
The findings underscore how obesity not only increases the risk of developing cancer but may also make tumors more aggressive once they form. By identifying the biological conversation between fat cells and tumor cells, researchers hope to develop new strategies to disrupt this exchange and improve outcomes for patients.
