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. 2021 Feb 20;296:100445. doi: 10.1016/j.jbc.2021.100445

Figure 5.

Figure 5

TANC2-PRKCA-expressing cells exhibit reduced levels of cleaved caspase-3 and decreased apoptosis.A, immunoblot analysis of lysates from parental, CRISPR-edited TANC2-PKCα fusion, and heterozygous PKCα knockout cells, probed for caspase-3, cleaved caspase-3, PKCα, and β-actin. Data are representative of three independent experiments. B, apoptosis assay performed on MDA-MB-231 parental (gray), CRISPR-edited TANC2-PKCα fusion (purple), or heterozygous PKCα knockout (orange) cells. Data represent luminescence upon binding of annexin V-luciferase to cell-surface-exposed phosphatidylserine as a function of time following addition of reagents. Graph depicts mean ± SEM from three independent experiments. ∗∗p < 0.01, ∗∗∗p < 0.001 (Student’s t-test). Asterisk indicates significance between parental and fusion-expressing cells, and # indicates significance between parental and heterozygous PKCα knockout cells. C, apoptosis assay described in (B) was performed on MDA-MB-231 parental (gray), CRISPR-edited TANC2-PKCα fusion (purple), or heterozygous PKCα knockout (orange) cells treated with etoposide (12.5 μM) or vehicle (DMSO) for 24 h. Graph depicts mean ± SEM from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 (Student’s t-test). Asterisk indicates significance between vehicle and etoposide-treated conditions for each cell line. # and % indicate significance between the parental and CRISPR-edited fusion or heterozygous PKCα knockout cells in basal and etoposide-treated conditions, respectively.