An international research team led by Justus Liebig University Giessen (JLU) has identified a promising therapeutic mechanism against lung cancer. The body’s own substance itaconate can reprogram macrophages in the tumor microenvironment and at the same time directly inhibit the growth of cancer cells.

The team led by Prof. Dr. Rajkumar Savai from the Institute of Lung Health (ILH) and JLU found that there is a deficiency of itaconate in lung cancer tumors. This deficiency leads to macrophages – immune cells with a dual role – switching to a tumor-promoting form. By increasing the itaconate concentration, it is possible to reprogram these cells into an anti-tumor form that slows down cancer growth.

In addition, a variant called octyl-itaconate acts directly on the tumor cells. It blocks the enzyme G6PD, which is crucial for the energy metabolism of cancer cells, and thus deprives them of the necessary “fuel” for multiplication.

The results showed that by specifically influencing the metabolism, both the immune system could be strengthened and the cancer cells directly weakened, the study said. The effect has also been demonstrated in human lung tissue samples.

Lung cancer is one of the most common and deadliest cancers worldwide. The new understanding of itaconate metabolism could form the basis for new drugs that starve tumor metabolism and activate the body’s own defenses.

The study was published in the journal “Cell Metabolism”. In addition to JLU and the ILH, the Max Planck Institute for Heart and Lung Research in Bad Nauheim, the German Center for Lung Research (DZL) and other international partners were involved in the work. The research was funded by the German Research Foundation (DFG), the state of Hesse and the European Union, among others.

Original Paper:

IRG1/itaconate rewires macrophage and lung tumor metabolism through G6PD inhibition: Cell Metabolism

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Editor: X-Press Journalistenbüro GbR

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