ITF2357 Induces Cell Cycle Arrest and Apoptosis in Meningioma Cells

Abstract As a type of central nervous system tumor, meningioma usually compresses the nerve center due to its local expansion, further causing neurological deficits. However, there are limited therapeutic approaches for meningiomas. ITF2357, a potent class I and II histone deacetylase inhibitor (HDACi), has been shown to inhibit cell proliferation, promote apoptosis and block the cell cycle in a variety of sarcoma cells, including glioblastoma and peripheral T-cell lymphoma. Here, we investigated the antitumor potential of ITF2357 on meningioma cells (IOMM). First, we demonstrated that the half-maximal inhibitory concentration (IC50) of ITF2357 was 1.842 µg/ml by MTT assay. In addition, ITF2357 effectively inhibited the proliferation and colonization ability of IOMM cells. Flow cytometry analysis showed that ITF2357 induced G0/G1 cell cycle arrest and cell apoptosis. Mechanically, the RNA sequencing data revealed that ITF2357 could affect the PI3K-Akt signaling pathway and the cell cycle progression. Furthermore, the expression level of cyclin B1, cyclin D1, and CDK1 was determined by western blotting. Collectively, our data revealed that ITF2357 inhibited cell viability and proliferation of meningioma cells by inducing G0/G1 phase arrest and apoptosis, and inhibiting cell cycle-related proteins (CDK/cyclin B1/cyclin D1), which developed a new approach to the treatment of meningioma.