Fig. 1

hCG prevents chemotherapeutic drug-induced decrease in tumor cell viability and apoptosis. a Cell viability analysis on B16, COLO-205, SP2/O and ChaGo-K-1 cells 24 h after hCG (10 μg/ml or ≅ 110 IU/ml) exposure. Means ± SEM of four independent experiments (with three replicates) are shown. For each cell line, data has been individually normalized to cells plus medium. (*p < 0.003, ^@p < 0.03, ^#p < 0.04, ^$p < 0.0003 vs cells plus medium). b Proliferative responses of B16, COLO-205, SP2/O and ChaGo-K-1 cells 24 h after hCG exposure. Means ± SEM of three independent experiments (with three replicates) are shown (*p < 0.0001, ^@p < 0.0001, ^#p < 0.0001, ^$p < 0.0001 vs cells without hCG). c Cell viability analysis of COLO-205 (left top and bottom panels) and SP2/O (right top and bottom panels) cells after pre-incubation with either medium or hCG for 24 h and then exposed to different concentrations of curcumin (for 24 h) or tamoxifen (for 48 h). VC: Vehicle control. Means ± SEM of four independent experiments (with three replicates) are shown. For each cell line and for both control cultures and cultures containing hCG, data has been individually normalized to cells plus vehicle control (VC). (*p < 0.04, ^#p < 0.009, ^$p < 0.0009 vs cells not exposed to hCG at the same drug concentration). d Reactivity of ChaGo-K-1, COLO-205, SP2/O and LLC1 cells towards Annexin-V-PE by flow cytometry post-exposure to two chemotherapeutic drugs (black profiles). In test cultures (green profiles), cells were exposed to hCG before addition of the drugs. Red profiles indicate secondary antibody controls. Representative profiles of three independent experiments are shown. e Levels of pro-caspase 3 and caspase 3 in ChaGo-K-1 cells treated with hCG, curcumin or with hCG + curcumin. Cytochrome c (CYT C) was employed as loading control