Fructose may enhance the spread of ovarian cancer: what a preclinical study found

• Ovarian cancer cells that survived chemotherapy released fructose, which enhanced the spread of tumor cells in a preclinical model.
• Fructose reduced cholesterol production in neighboring cells, weakening the connections between them.
• The effects of restricting fructose and using statins on patient outcomes were not established in the study provided.

Fructose as a signal for tumor cells

Researchers at the Wistar Institute described a possible role for fructose in the spread of aggressive ovarian cancer. According to their findings, some tumor cells that survived chemotherapy release this sugar into their surroundings. There, it acts not only as an energy source: in a preclinical model, fructose became a chemical signal that helped neighboring cancer cells acquire the ability to spread. The study was published in the journal Nature Aging.

What makes this observation notable is that cells that survive treatment may remain biologically active even if they no longer divide. The study’s first author, postdoctoral researcher Aidan Cole, described them as a source of molecular signals for neighboring cells. The study shows that these signals may include a nutrient—fructose. This broadens our understanding of how non-proliferating cells may influence tumor behavior after therapy.

The type of treatment and the nature of the disease are important clinical context. Most patients with ovarian cancer receive platinum-based drugs, which damage the DNA of cancer cells and prevent them from multiplying. Although many initially respond well to treatment, the cancer eventually returns in most cases. The disease also often spreads throughout the abdominal cavity; metastases account for about 90% of deaths from ovarian cancer.

What happens after chemotherapy

To test the role of cells that survived chemotherapy, the team separated them from the substances they released. In a preclinical experiment, the molecules alone—without the cells themselves—were enough to significantly increase the spread of cancer. This distinction matters: the result points to an effect of substances released by the cells, not just the effects of the surviving cells themselves. The authors describe this as one of the first observations of its kind in a preclinical model, rather than only in a laboratory dish.

The next step was to find out exactly which substances were linked to the change in tumor-cell behavior. The researchers identified fructose—a sugar that occurs naturally in foods such as fruit and honey. It is also found in regular table sugar and high-fructose corn syrup, which is used in sweetened drinks and processed foods. In the experiments, cells that survived chemotherapy produced fructose and released it into their surroundings.

In the mechanism described, fructose acts not merely as a nutrient but as a message to neighboring tumor cells. In response to this signal, they became more capable of spreading. This does not mean that fructose alone is the sole cause of metastasis: the study examines a specific cellular mechanism and the results of preclinical experiments. It offers an explanation for how cells may continue to affect other tumor cells after treatment.

How sugar affects cell adhesion

The researchers also reported that, in preclinical experiments, high fructose intake comparable to the amount found in sugary drinks could enhance signals associated with cancer spread, even without chemotherapy. This observation points to a possible mechanism linking diet and tumor behavior that was previously unknown. However, it does not prove that eating sugar causes cancer to spread in humans, nor does it allow the experimental results to be directly applied to patients.

The publication also notes the potential practical significance of diet: in the United States, high-fructose corn syrup may account for roughly 8–20% of daily calorie intake for some people. The authors point out that fructose consumption is a modifiable factor, so diet could become a focus of research into limiting tumor spread in the future. However, it has not yet been established whether reducing fructose intake improves treatment outcomes for patients with ovarian cancer.

To understand the cellular mechanism, the team examined changes in cancer cells exposed to fructose using several methods, including CRISPR screening. This approach makes it possible to systematically investigate genes and determine which ones affect a particular cellular process. In this case, the combined experiments pointed to reduced cholesterol production in neighboring tumor cells. This linked the fructose signal to a change in the cells’ properties, not just their energy metabolism.

Practical implications and unresolved questions

Cholesterol is needed for more than just the reasons it is usually discussed in relation to the heart. It is part of cell membranes—the outer layers involved in a cell’s interactions with its surroundings. In the mechanism studied, cholesterol helps maintain contact between neighboring cells. These connections act like a kind of biological glue, making it harder for cells to separate from one another. As a result, the reduction in cholesterol production caused by fructose weakened these contacts.

When the connections between tumor cells become weaker, individual cells may, according to the proposed mechanism, detach more easily. This could make it easier for them to leave the original site and spread elsewhere. In this way, the study links fructose, reduced cholesterol production, and weakened cell-to-cell contacts in a sequence of events. This is a possible explanation for a dangerous feature of ovarian cancer, not proof that this chain of events works the same way in all patients.

The finding about cholesterol also led the researchers to look at statins, widely prescribed drugs that lower cholesterol levels. The source says that around 39 million people in the United States take statins, but does not report that the study established any effect of these drugs on cancer spread or treatment outcomes. The link between taking statins and the mechanism described therefore remains a question for further investigation. Neither dietary recommendations nor conclusions about medications based on these findings have yet been confirmed by clinical data.

Source: ScienceDaily