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. 2019 Dec 6;11(12):1964. doi: 10.3390/cancers11121964

Figure 6.

Figure 6

Schematic diagram of the mechanism of HCPT on ESCC. HCPT blocked the combination between TOP I enzyme and supercoiled DNA, decreasing the enzyme activity of TOP I. Foci formation subsequently occurred to promote DNA damage. As a consequence, cell cycle transition was inhibited and the G2/M phase was arrested. All of these processes finally led to cell proliferation halt and cell apoptosis, as indicated by the decreasing Ki-67 expression as well as the changing apoptosis markers.