LiCl Treatment Induces Programmed Cell Death of Schwannoma Cells through AKT- and MTOR-Mediated Necroptosis.

In this study, we found that lithium chloride (LiCl) significantly inhibits the proliferation of both RT4 cells and human NF2-associated primary schwannoma cells by inhibiting the expression of apoptosis-related proteins. LiCl-induced cell death exhibits ultrastructural features of necrosis and is reversed by the RIPK1-specific inhibitor necrostatin-1 in a dose-dependent manner, indicating that LiCl induces the necroptosis type of cell death. Moreover, LiCl treatment induces ROS generation and activates the AKT/mTOR pathway, which is reversed by necrostatin-1 treatment. Based on our results, LiCl treatment may induce the programmed cell death of schwannoma cells through AKT- and mTOR-mediated necroptosis, potentially representing a new mechanism by which LiCl induces tumor cell death. Moreover, LiCl may prove to be a new drug for treating schwannoma. PMID: 28397069 [PubMed - as supplied by publisher]
Source: Neurochemical Research - Category: Neuroscience Authors: Tags: Neurochem Res Source Type: research