Figure 5
From: Targeting MKK3 as a novel anticancer strategy: molecular mechanisms and therapeutical implications
MKK3 depletion increases chemotherapeutic response in both wtp53 and mutp53 cancer cells. (a) Engineered sh/scr and sh/MKK3 HCT116 and HT29 cell lines were maintained in DOX condition for 48 h and treated/untreated for 24 h with ADR (1, 1.5, and 2 μM). Cells were then collected and protein lysates were analyzed by western blot analysis. The membrane was probed with specific anti-PARP and anti-β-actin (as loading control) antibodies. (b) Clonogenic survival assay of: HCT116 (left panel), MDA-MB468 (middle panel), and HT29 (right panel) sh/scr and sh/MKK3 cell lines, DOX-induced for 48 h and then treated with ADR 0.1 μM (HCT116 and MDA-MB468) or 0.5 μM (HT29) for 24 h. After treatment, the culture medium was replenished, and cells were maintained at 37 °C for 14 days. Grown colonies were stained with crystal violet. (c) Densitometric analyses of clonogenic assays as described in b. Plates were scanned and quantified by the ImageJ software. The graph shows the absolute values of plates densitometry. Plating was performed in triplicate
