Common Sugar Appears to Loosen Cancer Cells And Help Them Spread : ScienceAlert

Common Sugar Appears to Loosen Cancer Cells And Help Them Spread

Health10 August 2026By Starre Vartan

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Cancer cells secrete a cocktail of factors that affect how they grow and move. (Science Photo Library/Canva)

Cancer can be just like the killer in a horror movie – it may seem like he's been destroyed forever by the Good Guy, but then he pops back up again to terrorize.<br>Similarly, chemotherapy is designed to kill cancer cells, but some of them still survive treatment by entering a state known as cellular senescence.

Far from lying dormant, these cells remain metabolically active, releasing a mixture of proteins, fats, and other molecules that can reshape the tumor and its environment by signaling to nearby cells.

New research published in Nature Aging has just discovered that one of those signals might be the same stuff that's sitting in your kitchen cabinet, and it may be instructing cancer cells to spread.

"Our study is among the first to show that a nutrient – in this case, fructose – can act as one of those signals," says Aidan Cole, a molecular biologist at The Wistar Institute in Philadelphia.

Here's how they figured it out: The team focused on ovarian cancers treated with cisplatin, a powerful platinum-based chemotherapy that commonly induces cell senescence.

Although most patients initially respond well to treatment, recurrence is common, and then tumors spread throughout the abdominal cavity.<br>Senescent cancer cells are still metabolically active, releasing a mixture of molecules, collectively known as SASP (senescence-associated secretory phenotype), which affects neighboring cells. (Cole et al., Nature Aging, 2026)What causes those cells to move around?

If the researchers could understand that, it could provide a clue as to how they could prevent cancer recurrence – which is how 90 percent of the people who die from the disease are killed.

To determine what the cellular process was, the researchers first induced senescence in lab-grown ovarian cancer cells with cisplatin, then collected the growth media, which contained all the molecules the cells had released over two days.

Exposing untreated ovarian cancer cells to this media did not make them divide faster or become more resistant to cell death.

What the researchers saw was that it did make them much more likely to loosen their grip on neighboring cells and detach from three-dimensional tumor-like spheroids, the first critical step in ovarian cancer's characteristic mode of spread.

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When they heat-inactivated and filtered out suspect proteins, the effect persisted. So the researchers could eliminate well-known signaling molecules, such as cytokines and growth factors, which are both types of proteins.

It had to be a much smaller molecule.

Metabolic analyses pointed to fructose. Senescent cells consumed glucose but secreted elevated levels of fructose.

Simply adding physiological concentrations of fructose to otherwise normal conditioned media was enough to reproduce the increased cell detachment, while restoring glucose largely reversed the effect.

The researchers then worked through the metabolic cascade triggered by fructose. It didn't act only as a fuel; fructose altered mitochondrial metabolism, which ultimately reduced cholesterol production.

That loss of cholesterol had an important consequence, because it helps stabilize cell membranes and anchors cells to one another and to surrounding tissue. With less cholesterol in the membranes, cancer cells became less adhesive and more likely to break free.<br>Spheroid cell cultures detached when treated with the secretome of senescent cancer cells. (Cole et al., Nature Aging, 2026)The researchers first saw this detachment in cell culture, but looked at the process in mice, too.

Mice implanted with ovarian cancer cells developed substantially more metastatic tumors when treated with the senescent cells' material than with the same materials from normal cells, despite no increase in cancer cell proliferation.

And another important finding: Mice fed a high-fructose diet developed more widespread metastatic disease than animals receiving glucose.

And when the researchers disabled the cancer cells' ability to metabolize fructose, they found fewer cancer cells moving around.

This means that what an animal eats could influence how cancer progresses.

"As far as we know, this is the first time anyone has shown, in a preclinical model rather than just a dish, that it's the molecules these cells release – not the cells themselves – that drive the cancer's spread," Cole says.<br>It's important to note that these findings are preclinical – from mouse and cell experiments – and should not be...