Anti-cancer effects of dopamine in human glioma: involvement of mitochondrial apoptotic and anti-inflammatory pathways.

We report that dopamine inhibited glioma cell proliferation. We investigated the biological functions of dopamine via migration, colony formation and apoptosis assays in glioma cells. We also evaluated cytochrome c release from the mitochondria and p50 and p65 subcellular localization by fluorescence microscopy. We performed western blotting and real-time quantitative polymerase chain reaction to detect apoptosis and inflammatory marker protein and gene expression levels, respectively. NF-κB p50/p65 nuclear localization was analyzed after U87MG and U251 cells were treated with dopamine. The in vivo anti-tumor efficacy of dopamine was also analyzed in xenograft mice. Taken together, our results indicated that dopamine induced apoptosis by activating the cytochrome c and caspase-dependent apoptotic pathway. Moreover, dopamine markedly down-regulated inflammation-related protein expression levels and p50/p65 NF-κB nuclear localization in tumor cells, thereby inhibiting increases in tumor weight and size in xenograft mice. Thus, therapies targeting the mitochondrial apoptotic and anti-inflammatory signaling pathways regulated by dopamine may represent promising treatments for human glioma. PMID: 29179451 [PubMed]
Source: Oncotarget - Category: Cancer & Oncology Tags: Oncotarget Source Type: research