A team of researchers from the Federal Polytechnic School of Zurich (Switzerland) demonstrated in a study that the cancer cells of the skin can transfer their mitochondria to healthy connective tissue cells (fibroblasts) located in its immediate environment, using this mechanism as a strategy to obtain advantages and ensure its development.
The project, led by the Sabine Werner cell biology professor, revealed an unexpected resource through which some tumors guarantee their survival. Specifically, it was discovered that the malignant skin cells transmit their mitochondria to neighboring fibroblasts through small tubes formed by cell membranes, a process comparable to a pneumatic transport system.
“Cancer cells exploit a mechanism that is beneficial in case of injury for their own ends,” Werner said.
Mitochondria, organelles in charge of producing energy in the form of ATP, modify the behavior of fibroblasts once they are transferred. These become tumor -associated fibroblasts, characterized by rapid multiplication, greater ATP production and the secretion of growth factors and cytokines.
All this promotes the proliferation of tumor cells, which increase their aggressiveness. In addition, altered fibroblasts also change the composition of the extracellular matrix – essential structure for tissue stability – so that it further favors cancer expansion.
The finding occurred accidentally when the postdoctoral researcher, Michael Cangkrama, detected tiny tubular connections between cancer cells and fibroblasts in a joint laboratory crop. Subsequently, he was able to verify that these structures allowed the transfer of mitochondria.
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Mechanism is replicated in other types of cancer
Although it was already known that healthy cells could donate mitochondria in lesion contexts, such as after a stroke, had not been documented until now that malignant cells could transfer them in reverse sense to healthy cells.
Additional research confirmed that this mechanism is also present in breast and pancreas tumors, being especially relevant in the latter due to the large number of fibroblasts it contains.
In the molecular aspect, scientists identified the MIRO2 protein as a key element in this process. This protein appears at very high levels in cancer cells that transfer mitochondria, particularly on the invasive edges of tumors, where they are in close contact with fibroblasts. According to Werner, the results were consistent with what they expected to find.
The study opens new therapeutic perspectives. By blocking MIRO2 action in laboratory experiments and animal models, researchers managed to prevent mitochondrial transfer, which prevented fibroblasts from acquiring tumor promoting characteristics.
However, specialists warn that it is still necessary to identify a specific MIRO2 inhibitor with minimum side effects before being able to transfer this finding to clinical treatments.
“If they succeed, said inhibitor could be transferred to long -term clinical applications,” says Werner. However, they are likely to pass years before this type of therapy will be developed and tested.
With agency information
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