作者: Mrinmay Chakrabarti , Swapan K. Ray
DOI: 10.1016/J.GENE.2015.07.034
关键词: Stem cell 、 Angiogenesis 、 Apoptosis 、 Cell growth 、 Biology 、 mir-137 、 Transfection 、 Growth factor receptor 、 DNA methylation 、 Molecular biology
摘要: Glioblastoma is the deadliest brain tumor in humans. Recent studies suggested that 5-aza-2-deoxycytidine (AzaC) could inhibit cell cycle progression human glioblastoma stem cells by an indirect increase expression of suppressor microRNA-137 (miR-137). Delphinidin (DPN), a new anthocyanidin, inhibits growth different cancers. We investigated inhibition after or direct overexpression miR-137 and then DPN treatment. The highest occurred due to treatment with combination 10 μM AzaC 50 U87MG LN18 cells. methylation sensitive-polymerase chain reaction (MS-PCR) results showed inhibited promoter region, which was hypermethylated both lines, cause expression. Our also indicated transfection mimics Combination caused invasion prevented angiogenic network formation least factor (VEGF) co-culture microvascular endothelial This strategy most effectively survival factors (p-Akt NF-κB), (VEGF b-FGF), receptor (EGFR), invasive (MMP-9 MMP-2). Direct augmented efficacy induce apoptosis activation extrinsic intrinsic pathways. So, sequential be promising