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. 2020 Feb 29;48(8):4480–4491. doi: 10.1093/nar/gkaa127

Figure 3.

Figure 3.

Knockdown of HCP5 impairs DSBs HR repair and promotes apoptosis of GCs through MSH5. (A) Immunofluorescence showed the γH2AX foci formation in HCP5-silencing and negative control KGN cells suffered from ETO treatment. (B) After exposed to ETO for 6 h, the γH2AX levels were detected by western blot in HCP5-silencing and negative control KGN, COV434 and SVOG cells. Data shown represent three independent experiments. (C) Immunofluorescence showed the γH2AX foci formation in HCP5-silencing and negative control KGN cells suffered from CPT treatment. (D) After exposed to CPT for 2 h, the γH2AX levels were detected by western blot in HCP5-silencing and negative control KGN, COV434 and SVOG cells. Data shown represent three independent experiments. (E) Knockdown of HCP5 enhanced the cleavage of PARP and formation of γH2AX caused by treatment with Etoposide in KGN, COV434 and SVOG cells. Data shown represent three independent experiments.