fig2

Novel <i>N</i>-chloroacetyl-2-pyrazoline analogs with 2-naphthyl and ferrocenyl groups: targeting histamine receptor H1 to overcome colorectal cancer drug resistance

Figure 2. Clac10 (5c) and Clac12 (5e) cause cell cycle arrest in CRC cells. (A) HCT116 and (B) DLD1 cells were treated with IC50 and ½IC50 concentrations of 5c (Clac10) and 5e (Clac12) for 48 h and analyzed by flow cytometry after propidium iodide staining for DNA content; (C) The quantification figure shows that both compound treatments led to cell cycle arrest, as evidenced by an increase in the Sub-G0 cell population; (D) Lysates from HCT116 and DLD1 cells treated with IC50 concentrations of 5c (Clac10) and 5e (Clac12) for 48 h were examined by western blotting. Both compounds significantly reduced cyclin D1 expression. Data is presented as mean ± SD. An ordinary two-way ANOVA was used for statistical comparison. CRC: Colorectal cancer; IC50: half maximal inhibitory concentration; SD: standard deviation; ANOVA: analysis of variance; PI: propodium iodide.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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