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. 2016 Nov 3;291(50):26138–26150. doi: 10.1074/jbc.M116.737056

FIGURE 4.

FIGURE 4.

Knockdown of PKM2 enhanced cell cycle arrest in response to DNA damage. A, CCK-8 assay of cell proliferation in the NC or shPKM2#1-infected MCF7 cells for 5 days. Data are presented as means ± S.D. B–D, MCF7 (B), HCT116 (C), and U2OS (D) cells infected with NC or shPKM2#1 were exposed to a spectrum of etoposide for 3 days and were subjected to CCK-8 assay. **, p < 0.01 versus shPKM2#1. Data are presented as means ± S.D. E, MCF7 cells infected with NC or shPKM2#1 were treated with low dose (5 μm) of etoposide for 3 days before etoposide withdrawal. The cells were subjected to flow cytometry analysis at 0, 3, 6, 12 h after etoposide withdrawal. The quantification of G1 phase was shown. Data are presented as means ± S.D. F, MCF7 cells infected with NC, shPKM2#1 or/and shP21 were exposed to a spectrum of etoposide for 3 days and were subjected to CCK-8 assay. **, p < 0.01; *, p < 0.05 versus shPKM2#1/shP21. G, MCF7 cells infected with NC, shPKM2#1 or/and shP21 were treated with etoposide and subjected to Western blot analysis.