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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Targeting of tubulin polymerization and induction of mitotic blockage by Methyl 2-(5-fluoro-2-hydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylate (MBIC) in human cervical cancer HeLa cell

Fig. 4

a MBIC induced mitotic arrest: Western blot analysis was carried out to evaluate mitotic regulators levels after MBIC treatment. HeLa cells were treated with (0.21, 0.42 and 1 μM of MBIC. Figure a shows the evaluation of Cyclin B1, CDK1, mitotic checkpoint protein (BubR1) and a chromosomal passenger complex member, Aurora B. Samples were treated with colchicine (Col) and nocodazole (Noco) (at their IC50 concentration) as a positive control. β-actin served as a loading control. c, e MBIC induced mitochondria-dependent apoptosis: In order to evaluate whether MBIC caused mitochondria-dependent apoptosis, we evaluated anti-apoptotic protein Bcl-2, pro-apoptotic protein Bax, cleaved caspase-3/7/9 and cleaved PARP levels by western blot analysis (Fig. 4 c & e). HeLa cells were treated with MBIC (0.21, 0.42 and 1 μM). Samples were treated with colchicine (Col) and nocodazole (Noco) (at their IC50 concentration) as a positive control. β-actin served as a loading control. b, d & f The relative intensity of each protein was normalized with β-actin. Data were mean ± SD of three independent experiments. All the treatment groups were compared with control. “*” indicates statistically significant at P < 0.05

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