Figure 10.

Schematic of the proposed mechanism in this study. On one hand, TQ induces the overproduction of the intracellular ROS, which is closely associated with the mitochondrial dysfunction and MMP decrease. On the other hand, TQ blocks the cellular autophagic flux, resulting in the accumulation of autophagosomes. Together with the upregulated ROS, impaired autophagic flux activates the caspase dependent apoptosis, inhibiting the cancer progression. Nevertheless, whether intrinsic autophagic flux facilitates the cancer cells survival and cancer progression depends on the cell type and extent of activated autophagy, requiring further exploration. In addition, TQ upregulates the levels of hsa-miR-877-5p in 5637 and T24 cells, which decreases the level of PD-L1 protein, resulting in the attenuation of migration and invasion ability of BC cells. Arrows connecting different items present the inhibiting (red) or promoting (green) effect of various factors.