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. 2012 Feb 16;7(2):e32267. doi: 10.1371/journal.pone.0032267

Figure 2. PUMA knockout HCT-116 cells are partially resistant to BITC-induced apoptosis.

Figure 2

(A) Immunoblotting for PUMA protein using lysates from wild-type HCT-116 cells (WT) and PUMA knockout HCT-116 cells (PUMA KO) following 24 h treatment with DMSO or BITC (2.5 or 5 µM). (B) Quantitation of histone-associated DNA fragment release into the cytosol in WT and PUMA KO HCT-116 cells after 24 h treatment with DMSO or BITC (2.5 or 5 µM). Results are expressed as enrichment relative to corresponding DMSO-treated control. Data represent mean ± SD (n = 4). Significantly different (P<0.05) compared with arespective DMSO-treated control and bbetween WT and PUMA KO HCT-116 cells by one-way ANOVA followed by Bonferroni's multiple comparison test. (C) Visualization of apoptotic nuclei (DAPI assay) with condensed and fragmented DNA (identified by arrows) in WT HCT-116 cells after 24-hour treatment with DMSO or 5 µM BITC. (D) Quantitation of apoptotic nuclei in WT and PUMA KO HCT-116 cells following 24 h treatment with DMSO or BITC (2.5 or 5 µM). Data represent mean ± SD (n = 3). Significantly different (P<0.05) compared with arespective DMSO-treated control and bbetween WT and PUMA KO cells by one-way ANOVA followed by Bonferroni's multiple comparison test. Each experiment was repeated at least twice.