WeeklySA_AdminFACTOR: Scientists have found that the common sugar can act as a biological signal that helps aggressive ovarian cancer spread, opening new avenues for research into diet, chemotherapy and cancer treatment…
By Own Correspondent
Scientists have uncovered an unexpected link between fructose, a common dietary sugar, and the spread of aggressive ovarian cancer, raising fresh questions about the role of nutrition in cancer progression and the potential interaction between cholesterol-lowering drugs and chemotherapy.
The study, conducted by researchers at The Wistar Institute and published in Nature Aging, found that ovarian cancer cells surviving chemotherapy remain biologically active and release fructose, which acts as a chemical messenger encouraging neighbouring cancer cells to become more invasive.
Researchers say the findings provide one of the clearest indications yet that nutrients can directly influence the behaviour of cancer cells, although they caution that further clinical studies are needed before dietary recommendations can be made for patients.
“Our study is among the first to show that a nutrient—in this case, fructose—can act as one of those signals,” said lead author Dr Aidan Cole, a postdoctoral fellow in Professor Katherine Aird’s laboratory at The Wistar Institute.
Unlike healthy cells, chemotherapy-resistant cancer cells do not simply die or become inactive. Instead, they enter a dormant-like state in which they stop dividing but continue releasing molecules that influence surrounding tumour cells.
To investigate this process, researchers collected the substances secreted by chemotherapy-surviving ovarian cancer cells. When these molecules were introduced into laboratory models, neighbouring cancer cells became significantly more capable of spreading.
The discovery marks what researchers believe is the first demonstration in a preclinical model that substances released by treatment-surviving cancer cells—rather than the cells themselves—can actively promote metastasis.
Further investigation revealed fructose as the key signalling molecule responsible for this effect.
The findings also suggest that high dietary intake of fructose, particularly through sugar-sweetened beverages containing high-fructose corn syrup, may trigger similar biological pathways even in the absence of chemotherapy.
Because ovarian cancer frequently returns after initial treatment and typically spreads throughout the abdominal cavity, understanding what drives metastasis is considered critical.
Approximately 90% of ovarian cancer deaths are linked to metastatic disease rather than the primary tumour.
The researchers say the study highlights fructose as a potentially modifiable risk factor.
Unlike genetic predisposition or age, dietary fructose intake can be influenced by lifestyle choices. However, the team emphasises that no clinical trials have yet shown whether reducing fructose consumption can slow cancer progression in patients.
The researchers also uncovered an unexpected biological mechanism linking fructose to cancer spread.
Using large-scale genetic analyses, including CRISPR screening, they found that fructose suppresses cholesterol production inside neighbouring cancer cells. Cholesterol plays an important role in helping cells remain attached to one another. When cholesterol levels fall, cells lose this adhesive quality, making it easier for them to detach and migrate.
The finding has broader implications because millions of people worldwide take statins to reduce cholesterol.
Laboratory experiments found that statins alone also weakened the adhesion between cells, potentially making it easier for cancer cells to escape.
While the researchers stress there is currently no evidence that patients should discontinue cholesterol-lowering medication, they say the interaction between statins and chemotherapy deserves urgent investigation.
“We haven’t tested this effect in patients yet, but it raises questions about combining cholesterol-lowering drugs with chemotherapy, especially since ovarian cancer is most common in postmenopausal women who are often already on statins,” said Professor Katherine Aird, senior author of the study and co-leader of the Molecular and Cellular Oncogenesis Programme at The Wistar Institute.
The research team is now expanding its work to determine whether the same biological mechanism exists in other cancers that commonly spread within the abdominal cavity, including pancreatic, liver and colorectal cancers.
Although it is too early to conclude that fructose plays the same role across multiple cancer types, the scientists believe the mechanism may extend beyond ovarian cancer.
If confirmed in future studies, the discovery could reshape understanding of how diet, metabolism and cancer interact, while also informing future treatment strategies that combine chemotherapy with nutritional interventions and cholesterol-targeting therapies.
For now, researchers emphasise that the findings are based on preclinical studies and should not prompt patients to make changes to prescribed medications without consulting their healthcare providers. Instead, the study provides an important foundation for future clinical research into how diet and metabolism may influence cancer progression. – Science X
