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Fig. 1 | Molecular Cancer

Fig. 1

From: 3-BrPA eliminates human bladder cancer cells with highly oncogenic signatures via engagement of specific death programs and perturbation of multiple signaling and metabolic determinants

Fig. 1

Bladder cancer cells undergo cell type-specific and dose-dependent apoptotic and non-apoptotic death in response to 3-BrPA. (a, b and f) MTT cytotoxicity assays of RT4 (a), T24 (b) and T24-X (f) cells, grown at ~60 % confluency and treated with the indicated doses (μM) of 3-BrPA (stock in ddH2O) for 24 h (also, see Additional file 1: Figure S1 and Additional file 10: Table S2). (c) MTT cytotoxicity assays of T24 cells, grown at ~60 % confluency and treated with 125 μM of 3-BrPA for the indicated time periods (min). (d) MTT cytotoxicity assays of T24 and RT4 cells, seeded at the indicated confluency (low: ~30 %; medium: ~60 %; high: ~90 %) and exposed to 100 (T24) or 300 μM (RT4) of 3-BrPA, for 24 and 72 h, respectively. (a-d and f) Results are reported as mean ± standard deviation of triplicates of, at least, three independent experiments. *P < 0.001. (e) Representative flow cytometry charts (AnnexinV-FITC and 7AAD staining) of RT4 and T24 cells, grown at ~60 % confluency and treated with the indicated doses of 3-BrPA for 24 h. (g-h) Representative Western blotting profiles of whole-cell protein extracts obtained from RT4, T24 and T24-X cells, seeded at ~60 % confluency and exposed to the indicated doses of 3-BrPA for 24 h. The proteins examined were Caspase-8, Caspase-9, Caspase-3 (g), PARP, Lamin A/C and ICAD (h), while Actin was used as molecule of reference. Bracket and asterisk denote the high MW forms of ICAD protein (h). Flow cytometry (e) and Western blotting (g-h) experiments were repeated three independent times each

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