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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: ONC212, alone or in synergistic conjunction with Navitoclax (ABT-263), promotes cancer cell apoptosis via unconventional mitochondrial-independent caspase-3 activation

Fig. 1

ONC212 induce apoptotic cell death in HeLa and A549 cancer cells. a. The viability of HeLa was determined by MTT assay at different concentrations (5 to 20 μM) of ONC212 treatment for 48 h. The IC50 value was calculated to be 16.3 μM. b. A549 cell viability was assessed by MTT assay with ONC212 exposure (20 to 60 μM) for 48 h. The IC50 value was determined to be 54 μM. c. Hoechst-stained pictures of ONC212-induced nuclear condensation (20X objective, scale bar: 50 µm). Condensed nuclei are indicated by arrows. d. Percentage of condensed nuclei in random fields represented graphically (n = 3, mean ± SEM), **denotes p < 0.01 in control vs ONC212 treated cells (48 h). e & f. Representative flow cytometry scatter plots of Annexin-V FITC/PI staining in control and ONC212-treated cells. ONC212 treatment increased the proportion of early and late apoptotic cell populations compared to untreated control. g. Quantification of total apoptotic cells (Annexin V-positive, with or without PI positivity) expressed as a percentage of the total cell population. (n = 2, mean ± SEM), ** denotes p < 0.01 and *** denotes p < 0.001 in control vs ONC212 treated cells (48 h). h & i. Clonogenicity assay showing the survival efficacy of cancer cells after ONC212 treatment for 48 h. Cell density (displayed by crystal violet staining) was effectively reduced in ONC212-treated cancer cells than untreated control. Percentage of clonogenicity is assessed by colorimetric analysis of crystal violet staining and represented graphically (n = 3, mean ± SEM and **denotes p < 0.01) in both untreated vs treated

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