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. 2019 Apr 28;21(6):557–570. doi: 10.1016/j.neo.2019.03.011

Figure 2.

Figure 2

PCAF knockdown enhances the chemoresistance of HCT116 cells to 5-FU. (A) Knockdown of PCAF increases the clonogenicity of HCT116 cells. Clonogenic formation assay was used for determining the clonogenicity of HCT116 cells treated with 5-FU (1 μg/mL) (left panel). The quantitative results show the average percentage of surviving colonies (right panel). (B) PCAF knockdown increases chemoresistance of HCT116 cells to 5-FU. Cell viability of HCT116 cells treated with 5-FU (2 μg/mL) for 48 h was determined by CCK8 assay. (C) PCAF knockdown decreases the amount of cleaved caspase-3 and cleaved PARP induced by 5-FU (5 μg/mL) treatment (left panel). Quantitative analysis of protein level changes in HCT116 cells by measuring the intensity of western blot band (right panel). The data are means ± SD of three independent assays, *: P < .05 vs. NS, #: P < .05 vs. Ctrl, n = 3. (D) PCAF knockdown reduces apoptosis of HCT116 cells induced by 5-FU. AO/EB staining was used for measuring apoptotic cell population in HCT116 cells treated with 5-FU (5 μg/mL) (left panel). The quantitative results show the average percentage of apoptotic cells from 3 images taken from each group (right panel). (E) PCAF knockdown attenuated the 5-FU-induced apoptosis of HCT116 cells. Annexin V-PI dual staining-based flow cytometry assay was used for measuring apoptotic cell population in HCT116 cells treated with 5-FU (5 μg/mL). The total number of cells in the Q2 and Q4 quadrant was regarded as apoptotic cells. Percentages of apoptotic cells are shown in the bar graph. The data are means ± SEM of three independent assays. *: P < .05 vs. NS. #: P < .05 vs. Ctrl. (n = 3).