Cancer Breakthrough in Hungary Identifies Switch to Inhibit Tumour Growth
- 17 Jul 2026 11:14 AM
Researchers at Eotvos Lorand University have identified a molecular switch that inhibits tumour growth by disrupting the synthesis of fatty acids in cancer cells.
The study found that blocking a specific enzyme triggers changes in the metabolism of cancer cells, stopping tumour growth regardless of insulin levels.
Cancer cells typically reprogramme their metabolism to accelerate the production of biomolecules such as nucleic acids, proteins, and lipids, which are essential for their rapid growth and division.
The research team which also includes the HUN-REN Biological Research Centre's Institute of Biochemistry in Szeged, sought to understand why tumours increase their own fatty acid synthesis instead of absorbing lipids from the bloodstream and whether these locally produced molecules have additional roles beyond construction.
The team, whose corresponding author is Szabolcs Takats, used fruit fly models to conduct functional genetic tests. They found that the enzyme ACC, which regulates the first key step in fatty acid production, is essential for the rapid growth of late-stage tumours.
When ACC is inhibited, the composition of fats and lipid molecules in the tumour changes dramatically, depleting locally produced fatty acids and replacing them with highly unsaturated fatty acids from food or host tissues.
This shift can alter the composition and function of cell membranes.
The researchers also discovered that disrupting fatty acid synthesis directly deactivates the TORC1 protein complex, which plays a central role in sustaining cell growth. When TORC1 signalling is halted, cell growth stops, and self-destruct processes are triggered.
This finding is particularly significant because excessive activity of the insulin and TORC1 pathways in many human tumours not only drives rapid growth but also contributes to resistance against conventional therapies.
The results suggest that ACC inhibitors could serve as effective complementary therapies for tumours with heightened insulin-TORC1 signalling.
This could be especially valuable for tumours that have become resistant to insulin signalling inhibitors, as direct ACC inhibition may offer a new intervention point.
The study's findings have been published in the journal Cell Death and Disease.
Photo: Pixabay
Source: MTI – Hungary’s national news agency since 1881.
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