Nicotinic receptors modulate antitumor therapy response in triple negative breast cancer cells

Figure 6 Effect of paclitaxel and nicotine on MDA-MB-231 cell viability. A: Cells were treated with paclitaxel (PX) (10^-7 mol/L) and the mediators were evaluated in the absence or presence of the kinase inhibitors for: PKC (staurosporine, 10^-8 mol/L), MEK (PD098059 PD, 10^-5 mol/L), Ras (S-trans, trans-farnesylthiosalicylic acid, 10^-6 mol/L), ERK1/2 (U126, 10^-5 mol/L), p38MAPK (SB203580, 10^-5 mol/L) or IKKβ (IMD354, 5 × 10^-8 mol/L); B: Cells were treated with the combination of PX and nicotine (NIC) (10^-10 mol/L) as well as with the same inhibitors as those shown in Figure 6A. Values are the mean ± SD of four experiments performed in duplicate. ^aP < 0.05; ^bP < 0.01 vs PX. ^cP < 0.05; ^dP < 0.01; ^eP < 0.001 vs PX+NIC. FTS: S-trans, trans-farnesylthiosalicylic acid; SB: SB203580; Stau: Staurosporine; PD: PD098059; PX: Paclitaxel; NIC: Nicotine.