Peptide gomesin triggers cell death through L-type channel calcium influx, MAPK/ERK, PKC and PI3K signaling and generation of reactive oxygen species
作者： Vivaldo Moura-Neto , Manuela G. Lopez , Nelson H. Gabilan , Rossana C. Soletti , Laura del Barrio
DOI: 10.1016/J.CBI.2010.04.012
关键词:
摘要: Gomesin is an antimicrobial peptide isolated from hemocytes of a common Brazilian tarantula spider named Acanthoscurria gomesiana. This exerts antitumor activity in vitro and vivo by unknown mechanism. In this study, the cytotoxic mechanism gomesin human neuroblastoma SH-SY5Y rat pheochromocytoma PC12 cells was investigated. induced necrotic cell death to cells. The evoked rapid transient elevation intracellular calcium levels Fluo-4-AM loaded cells, which inhibited nimodipine, L-type channel blocker. Preincubation with nimodipine also Gomesin-induced prevented pretreatment MAPK/ERK, PKC or PI3K inhibitors, but not PKA inhibitor. addition, generated reactive oxygen species (ROS) were blocked inhibitors. Taken together, these results suggest that could be useful anticancer agent, cytotoxicity implicates entry through channels, activation signaling as well generation species.
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