Fig. 6

The schematic diagram illustrates the hypothetical mechanism of action of Tu in MDR GC cells. As previously reported, aberrant glycosylation contributes to chemoresistance. For example, some types of glycosylation are upregulated in MDR cells [13, 14]. Moreover, dysregulated glycosylation leads to basal ER stress in MDR GC cells. Tu further exacerbates ER stress by inhibiting N-glycosylation, and excess ER stress subsequently activates apoptosis signaling, which decreases the chemoresistance of MDR cells to some extent. However, autophagy triggered by ER stress partially dampens the apoptosis-inducing effects of Tu