Omeg@Silica microparticles modulates p53 and cell proliferation in A549.

P53, a key tumor suppressor, in addition to controlling cell proliferation, represents a challenging target for anticancer drugs. Actin is an essential element of the cytoskeleton that is essential in ROS production and its polymerization increases along with p53 cellular accumulation in response to DNA damage agents or to apoptotic stress. Omeg@Silica, mesoporous silica functionalized with whole fish oil (FOS), exert anti-tumor effects on Non-Small Cell Lung cancer (NSCLC) affecting mitochondrial function, cell growth ability and apoptosis Aims: the present study was assessed to better understand the mechanisms by which Omeg@Silica exerts anti-cancer effects in NSCLC, exploring P53 expression, the actin polymerization, the cell proliferation, and the ability to form colonies of A549 cells. Methods: We treated adenocarcinoma cells (A549) with AnchoisOil dispersed in ethanol (10 mg/ml) or encapsulated in silica (FOS). We evaluated nuclear and cytoplasmic expression of p53 by western blotting. Actin polymerization was assessed evaluating phalloidin expression (flow cytometry). Cell proliferation was assessed by CFSE (flow cytometry) and by clonogenic assay. Results: We showed that FOS significantly increased nuclear p53 nuclear expression and actin polymerization while they significantly reduced cytoplasmic p53 and cell proliferation. Conclusion: These results suggest, for the first time, that Omeg@Silica microparticles could carry out their anti-cancer activity, increasing nuclear p53- along with an increase in F-actin polymerization that in turn could induce cell cycle arrest and cell apoptosis.