Journal
ONCOLOGY REPORTS
Volume 37, Issue 5, Pages 2829-2838Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2017.5562
Keywords
sulforaphane-cysteine; ERK1/2; cleaved caspase 3; apoptosis; glioblastoma
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Funding
- National Natural Science Foundation of China [81272843, 81601993]
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We previously demonstrated that sulforaphane (SFN) inhibited invasion via sustained activation of ERK1/2 in human glioblastoma cells. However, sulforaphane-cysteine (SFN-Cys), an analog of SFN, enriched in plasma with longer half-life, had more potentiality to induce apoptosis. Here we investigated the molecular mechanisms of SFN-Cys-induced apoptosis in human glioblastoma U373MG and U87MG cells. Cell viability assay showed that SFN-Cys inhibited cell viability in a dose-dependent manner. Cell morphology observation also showed SFN-Cys increased the phenotype of cell death in a dose-dependent manner. Furthermore, flow cytometry assay showed that SFN-Cys induced apoptosis significantly in a dose-dependent manner in both cell lines. Furthermore, western blot analysis demonstrated that SFN-Cys induced activation of ERK1/2 in a sustained manner and the activation contributed to upregulation of Bax/Bcl-2 ratio and cleaved caspase 3, and these results can be reversed by the ERK1/2 blocker PD98059. Our results showed that SFN-Cys induced cell apoptosis via sustained activation of ERK1/2 and the ERK1/2 mediated signaling pathways such as activation of caspase 3 and apoptosis-related proteins, thus indicating that SFN-Cys might be a more promising therapeutic agent versus SFN to resist glioblastoma cells, especially in Taxol-resistant cancer cells.
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