Renjith Vijayakumar Selvarani, Founder, Chairman, Chief Scientific and Technology Officer at Olusium, and Co-Principal Investigator at Cancer Institute (WIA), shared on LinkedIn:
“Fructose as a Metabolic Driver of Cancer Cell Dissemination and Metastatic Progression.
Scientists have uncovered an unexpected culprit in cancer progression: fructose.
A fascinating study from The Wistar Institute has revealed a surprising mechanism that may help explain how high-grade serous ovarian cancer can return and spread after chemotherapy.
Chemotherapy is designed to kill cancer cells, but some cells survive by entering a state called senescence. These cells may stop dividing, but they are far from inactive.
Researchers found that chemotherapy – surviving senescent cells continue communicating with surrounding cancer cells by releasing a mixture of signaling molecules.
One of the most unexpected signals was fructose.
In preclinical models, senescent cells released fructose, which altered cholesterol levels in neighboring cancer cells.
This reduced their ability to remain attached to one another, potentially making it easier for individual cancer cells to detach, migrate, and metastasize.
What makes this finding particularly interesting is that it shifts attention beyond traditional protein – and gene – centered mechanisms toward metabolites as active drivers of cancer progression.
The study raises an important question:
Could targeting fructose metabolism help prevent cancer cells from acquiring properties that promote metastasis?
At the same time, it is important not to overinterpret the findings. The evidence is currently preclinical, and this does not establish that eating fructose or drinking sugary beverages directly causes ovarian cancer to spread in patients.
More research is needed to determine whether dietary fructose influences this pathway in humans and whether drugs targeting fructose metabolism could have therapeutic value.
Nevertheless, the study highlights something increasingly important in cancer, biology: cancer is not driven only by genes and proteins – metabolism and the tumor #microenvironment can also profoundly influence how cancer survives, adapts, and spreads.”
