New Delhi: Fructose has long been studied as a source of energy. Now, scientists say it may have another role inside tumours — as a molecular messenger that helps cancer spread. A new study has found that ovarian cancer cells surviving chemotherapy release the common sugar to prompt neighbouring tumour cells to break away, potentially aiding metastasis.
The findings, published in the journal Nature Aging by researchers at The Wistar Institute on 30 July, uncover a previously unknown way chemotherapy surviving cancer cells may contribute to the return of ovarian cancer. However, the researchers caution that the work is still at the preclinical stage and has not yet been confirmed in patients.
Ovarian cancer is one of the deadliest cancers among women because it frequently returns after treatment and spreads throughout the abdominal cavity. While most patients initially respond well to platinum-based chemotherapy, metastasis accounts for nearly 90 per cent of deaths from the disease.
Researchers found that not all cancer cells that survive chemotherapy remain inactive. Instead, some continue releasing a mix of molecules that influence nearby tumour cells.
To test their role, the team separated chemotherapy-surviving cells from the substances they secreted and exposed other ovarian cancer cells to those molecules. Even without direct contact with the surviving cells, the recipient cancer cells became significantly more invasive.
By analysing the secreted molecules, the researchers identified fructose as a key driver. It functioned as a chemical signal that encouraged neighbouring tumour cells to loosen their grip on one another and prepare to spread.
The study also explains how this happens. Using CRISPR-based genetic screens and other analytical techniques, the researchers found that fructose suppresses cholesterol production inside neighbouring cancer cells. Cholesterol helps cells remain attached to one another, acting like a biological glue. When cholesterol levels fall, those cellular bonds weaken, allowing cancer cells to detach more easily and spread through the abdominal cavity.
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New concerns
The findings also raise questions about diet and commonly prescribed cholesterol-lowering drugs. In preclinical models, dietary fructose at levels comparable to those found in sugary drinks was enough to promote cancer spread even in the absence of chemotherapy. The researchers say this suggests nutrition could influence cancer progression.
The same mechanism also drew attention to statins, which lower cholesterol production. In laboratory experiments, statins weakened the connections between cancer cells and made them easier to separate. However, the researchers stressed that the findings are preliminary and should not prompt patients to stop taking prescribed medication.
“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 Katherine Aird, senior author of the study.
The team is now investigating whether the same fructose-driven pathway could also influence the spread of other cancers, including pancreatic, colon, and liver cancers.
(Edited by Aamaan Alam Khan)