Ricerc@Sapienza

Several studies have been performed with the aim of identifying drugs able in inhibiting Epithelial-Mesenchymal Transition (EMT), chiefly by blocking PI3K/Akt pathway. We have already demonstrated that treatment with myo-Inositol at the pharmacological dose can block EMT in breast cancer cells by downregulating PI3K/Akt and inducing changes in cytoskeletal architecture. Herewith, we investigated the mechanism of action of myo-inositol in both highly (MDA-MB-231) and low (MCF-7) invasive human breast cancer cells.

Background: Several researches have been performed with the aim of identifying drugs able in blocking PI3K/Akt pathway. We have already demonstrated that myo-Inositol (myo-Ins) treatment can block EMT in breast cancer cells by downregulating PI3K/Akt and inducing changes in cytoskeletal architecture. Aim: Herein, we set our experiments to investigate migration/invasiveness inhibition though in vitro and in vivo models upon myo-Ins administration.

Inositol and its phosphate metabolites play a pivotal role in several biochemical pathways and gene expression regulation: inositol pyrophosphates (PP-IPs) have been increasingly appreciated as key signaling modulators. Fluctuations in their intracellular levels hugely impact the transfer of phosphates and the phosphorylation status of several target proteins. Pharmacological modulation of the proteins associated with PP-IP activities has proved to be beneficial in various pathological settings.