© HASANOVIC et al./IPMC Left: the Patched protein (in blue) expels some of the doxorubicin (Dxr) from the cancerous cell, and creates resistance to chemotherapy. Right: Patched remains inactive in the presence of methiothepin (in green), and the accumulation of doxorubicin in the cancerous cell leads to its death.
A team of researchers from the CNRS and Université Nice Sophia Antipolis
1 has just shown that a small molecule called methiothepin can inhibit the chemotherapy resistance of certain tumors. These results will be on the cover of the July 1, 2018 issue of International Journal of Cancer . Cancerous tumors are also capable of “detoxing,” subsequently limiting the efficiency of chemotherapy. To better understand this phenomenon, a team from Institut de pharmacologie moléculaire et cellulaire (CNRS/Université Nice Sophia Antipolis) studied the Patched membrane protein, and showed that this protein is capable of expelling some of the primary active ingredients of chemotherapy from cancerous cells. The rejection of these toxic substances enables the tumor to eventually survive the treatment. The Patched protein normally participates in embryonic development, but it is diverted as a tool for “detoxification” in numerous cancers: melanoma, adrenocortical carcinoma, colorectal cancer, breast cancer… After demonstrating that Patched actively contributes to resistance to doxorubicin, one of the medicines used in chemotherapy, researchers studied its inhibition through a small molecule called methiothepin. Remarkably, a combination of doxorubicin and methiothepin eliminates tumors more efficiently than doxorubicin alone, both in vitro on cancerous human cells, and in vivo on these same cells grafted in mice.
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