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Ruptures in cell nuclei enhance tumor invasion in Breast Cancer

The nucleus of a cell serves an important function: it protects the cell's DNA and allows it to be used properly. However, if the cell itself is compressed and deformed, such as during migration or proliferation, it can be damaged, if not temporarily shattered. DNA damage occurs as a result of the compression. As a result, healthy cells age faster and breast cancer cells acquire invasive qualities, as recently demonstrated by a research team from the CNRS, Institute Curie, and INSERM.

These researchers discovered that when cells are crushed and the nucleus is broken, DNA can come into contact with TREX1, a DNA-destructing enzyme. The normal job of TREX1 is to protect the cell by destroying the DNA of viruses that try to infect it, but also targets the cell DNA in these exceptional circumstances.

The cells in healthy tissue then show indications of aging and stop proliferating. However, the researchers discovered that in a breast tumor, the damage caused by TREX1 causes the cancer cells to become more invasive, rather than destroying them. When a tumor gets too large, for example, the cells become squeezed and gain the ability to destroy their environment, allowing them to infect neighboring tissues, increasing the risk of metastasis.

These findings highlight the significance of the TREX1 enzyme in the development of breast cancer as well as in the aging process. Scientists are now trying to find and test chemicals that could stop it from working. Because TREX1 plays such a crucial role in inflammation and immunity, these inhibitors could have a wide range of therapeutic applications.

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