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. Author manuscript; available in PMC: 2020 Sep 16.
Published in final edited form as: Blood Cancer Discov. 2020 Sep;1(2):198–213. doi: 10.1158/2643-3230.BCD-19-0077

Figure 2.

Figure 2.

APOC2 knockdown inhibits AML cell survival and induces apoptosis in vitro. Cell proliferation assays in MOLM-13 cells (A), THP-1 cells (B), and HL60 cells (C) infected with two different tet-on APOC2-shRNAs or control shRNA. The knockdown efficiency of APOC2 was measured by qPCR (compared by two-way ANOVA). D, Cell viability assay results for the knockdown of APOC2 in primary blasts from patients with AML. E, Colony formation assay results for the knockdown of APOC2 in AML primary blasts. F, Measurement of APOC2 knockdown in patient blasts by qPCR. G and H, Annexin V and PI staining levels were measured by flow cytometry to assess cell apoptosis in MOLM-13 and THP-1 cells infected with APOC2 shRNA or control shRNA. The quantification of early and late apoptotic cell population changes is presented in the panel on the right. The differences between the groups were analyzed using unpaired t tests (****, P < 0.0001; ***, P < 0.001; **, P < 0.01; *, P < 0.05; ns, not significant).