Fig. 11. The proposed mechanism of BITC-induced cytotoxicity through autophagy inhibition and lysosomal dysfunction in AGS cells. In human gastric adenocarcinoma AGS cells, BITC induced cell death by caspase-dependent apoptosis and inhibition of cytoprotective autophagy. It inhibited autophagy degradation through lysosomal dysfunction, which decreased both the quality and quantity of cathepsin proteins. Moreover, BITC may inhibit the autophagy initiation and elongation steps, since it decreased the expression levels of Beclin1, Atg5-Atg12 complex, and class III PI3K proteins. However, because of increased mRNA transcription and decreased lysosomal degradation, BITC also caused the accumulation of LC3B and p62. Nevertheless, there was no direct relationship between BITC-induced LC3B II accumulation and cytotoxicity.
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