Detailed Abstract
[Poster - Basic Research]
[P133] Dioscin induces gallbladder cancer apoptosis by inhibiting ros-mediated pi3k/akt signalling
Xiaoling SONG, Yingbin LIU
Department of General Surgery and Laboratory of General Surgery, Shanghai, China, China
Introduction : Gallbladder cancer (GBC), highly aggressive form of cancer with an extremely poor prognosis, is the most common malignancy of the biliary tract. Dioscin (DSN), a plant glucoside saponin, has been shown to exert many biological and pharmacological effects. However, the effect of dioscin on GBC remains unclear.Shanghai Key Laboratory of Biliary Tract Disease Research
Methods : A Cell Counting Kit-8 (CCK-8) assay and colony formation assay were used to evaluate NOZ and SGC996 cell viability. Antitumor activity through induction of apoptosis was by Annexin V/PI staining assay for apoptosis. DSN-induced mitochondrial dependent apoptosis was analysed by hoechst 33342 staining, mitochondrial membrane potential (ΔΨm) assay and treatment in the presence or absence of Z-VAD-FMK. The mechanisms of DSN-induced apoptosis was analyzed by reactive oxygen species (ROS) and glutathione (GSH) detection and western blot analysis. In vivo tumour xenograft study was used to evaluate the anti-cancer effects of DSN in vivo.
Results : The results showed that DSN significantly inhibited GBC cell proliferation and migration. Moreover, DSN induced GBC cell apoptosis via mitochondrial dependent apoptotic signalling. ROS and GSH levels were measured, and ROS scavengers completely inhibited DSN-induced apoptosis and migration. Western blot analysis showed that protein kinase B (AKT) activity was significantly downregulated after DSN treatment, and that inhibition/ectopic expression of AKT enhanced/abolished DSN-induced apoptosis but not migration. Furthermore, we confirmed the relationship between ROS and the PI3K/AKT pathway and found that DSN induced apoptosis by regulating ROS-mediated PI3K/AKT signaling.
Conclusions : DSN induces GBC apoptosis through inhibiting ROS-mediated PI3K/AKT signalling and suppressing GBC cell migration.
Methods : A Cell Counting Kit-8 (CCK-8) assay and colony formation assay were used to evaluate NOZ and SGC996 cell viability. Antitumor activity through induction of apoptosis was by Annexin V/PI staining assay for apoptosis. DSN-induced mitochondrial dependent apoptosis was analysed by hoechst 33342 staining, mitochondrial membrane potential (ΔΨm) assay and treatment in the presence or absence of Z-VAD-FMK. The mechanisms of DSN-induced apoptosis was analyzed by reactive oxygen species (ROS) and glutathione (GSH) detection and western blot analysis. In vivo tumour xenograft study was used to evaluate the anti-cancer effects of DSN in vivo.
Results : The results showed that DSN significantly inhibited GBC cell proliferation and migration. Moreover, DSN induced GBC cell apoptosis via mitochondrial dependent apoptotic signalling. ROS and GSH levels were measured, and ROS scavengers completely inhibited DSN-induced apoptosis and migration. Western blot analysis showed that protein kinase B (AKT) activity was significantly downregulated after DSN treatment, and that inhibition/ectopic expression of AKT enhanced/abolished DSN-induced apoptosis but not migration. Furthermore, we confirmed the relationship between ROS and the PI3K/AKT pathway and found that DSN induced apoptosis by regulating ROS-mediated PI3K/AKT signaling.
Conclusions : DSN induces GBC apoptosis through inhibiting ROS-mediated PI3K/AKT signalling and suppressing GBC cell migration.
SESSION
Poster
Poster / Exhibition Hall and Lobby(2F) 1/1/1970 9:00 AM - 9:00 AM