Skip to main content
. 2019 May 13;14:3491–3502. doi: 10.2147/IJN.S193192

Figure 1.

Figure 1

Schematic representation of inhibitory mechanism of nano-β-TCP on hepatocellular carcinoma. Intratumor injection of nano-β-TCP was performed on the xenograft hepatocellular carcinoma model. Nano-β-TCP was internalized into tumor cells by nonspecific endocytosis and rapidly degraded in the acidic lysosome to release Ca2+ and PO43- ions (①). Cell apoptosis was activated by extrinsic and intrinsic apoptosis pathways synergistically orchestrated with the ROS generation (②). In addition, the expression of some related cyclins (CyclinD1, CDK2, CyclinE, and β-catenin) was inhibited, eventually leading to cell cycle blocking in G0/G1 phase (③).