Anti-BAX monoclonal antibody

The discovery of alternative signaling pathways that regulate cell death has revealed multiple strategies for promoting cell death with diverse consequences at the tissue and organism level. Despite the divergence in the molecular components involved, membrane permeabilization is a common theme in the execution of regulated cell death. In apoptosis, the permeabilization of the outer mitochondrial membrane by BAX and BAK releases apoptotic factors that initiate the caspase cascade and is considered the point of no return in cell death commitment. Pyroptosis and necroptosis also require the perforation of the plasma membrane at the execution step, which involves Gasdermins in pyroptosis, and MLKL in the case of necroptosis. Although BAX/BAK, Gasdermins and MLKL share certain molecular features like oligomerization, they form pores in different cellular membranes via distinct mechanisms. Here, we compare and contrast how BAX/BAK, Gasdermins, and MLKL alter membrane permeability from a structural and biophysical perspective and discuss the general principles of membrane permeabilization in the execution of regulated cell death.

C21 steroidal glycosides have been extensively reported for treating several types of cancer and are widely found in Marsdenia tenacissima. In this study, a C21 fraction was synthesized from M. tenacissima, and its anti-cancer potency was assessed against in vitro gastric cell lines BGC-823, SGC-7901, and AGS. Significant growth inhibition and cell cycle arrest were observed in C21 fraction-treated gastric cancer cells. The results of apoptotic staining techniques in C21 fraction-treated gastric cells were confirmed with excess reactive oxygen species generation. Moreover, SOD and H2O2 levels were increased by C21 fraction, especially when combined with chloroquine (CQ). The apoptotic inducing potential of C21 fraction was also evidenced by upregulation of proapoptotic proteins cleaved-PARP and BAX and downregulation of antiapoptotic proteins Bcl-2 and p-AKT by western blot, especially in the presence of the autophagy inhibitor CQ. The results showed that the apoptosis of gastric cancer cells caused by C21 fraction was enhanced by inhibiting autophagy. The current findings reveal a new mechanism for the antitumor activity of C21 fraction on gastric cancer.