As we age our bodies change: the responsibility for this lies with the senescent cells, which have lost physiological functionality, stopped dividing and therefore proliferating. These cells can favor the onset of tumors. As we know, however, not everyone develops neoplasms and those who do have different prognoses. VIMM Principal Investigator Andrea Alimonti, in collaboration with an international team, has discovered a crucial genetic variable capable of acting on these cells, inhibiting or promoting the development of prostate cancer.
In a study just published in Cancer Cell, the professor and his team demonstrated the role of a gene that, if present in these cells, can counteract the metastatic process in prostate cancer. In the absence of this gene, on the contrary, the process is favored and therefore the patient’s prognosis is worse. However, VIMM researchers have developed a powerful senolytic compound that in the second option can remedy it, blocking neoplastic progression.
The gene in question is TIMP1, to which another one is added, PTEN, which plays an important role in the tumor process. In their experiment on genetically modified mouse models, Alimonti and colleagues suppressed the expression of TIMP1 and PTEN and thus witnessed the consequent development of metastases. At that point they used the senolytic compound. It is a substance that kills senescent cells and is therefore able to slow down aging. As a result, the researchers observed the blocking of metastatic progression.
This study therefore represents an important milestone in the search for a cure for prostate cancer. Explains Professor Alimonti, “these results direct us once again towards personalized therapy. Genetic factors can in fact determine whether senescence will have a positive effect on the patient, in opposition to tumor growth, or negative, in stimulating the formation of metastases. In this second case, it is important to carefully administer the chemotherapy drugs that induce senescence, as well as using senolytic drugs to kill senescent cells “.