Top 20 pharmaceutical perturbagens exhibiting positive correlation to the gene signature induced by Cud C treatment.

<p>Top 20 pharmaceutical perturbagens exhibiting positive correlation to the gene signature induced by Cud C treatment.</p

Cudraflavone C inhibits PI3K activity.

<p>The effect of negative control (1%DMSO), Cud C or LY-294002 (100 μM) on p110α/p85α, p110β/p85α, p110δ/p85α, and p120γ PI3K activity were quantified using the PI3K-Glo^™ Class I Profiling Kit. All data represents the mean ± s.d. from at least three independent experiments. Symbol “*” presents the statistical significance concluded from Student’s independent <i>t</i>-test with p-value ≤0.05.</p

Cudraflavone C induces tumor-specific cell death in colorectal cancer cells.

<p>(A) Chemical structure of Cud C. (B) KM12, HT29, Caco-2, HCC2998, HCT116 and SW48 colorectal cancer cells were exposed to various concentrations of Cud C for 72 hours. Cell viability was recorded using CellTitre Glo^® luminescence assay. (C) KM12, Caco-2 and CCD 841 CoN were treated with 0.1% DMSO (control) or 10μM Cud C (Cud C) for 72 hours followed by microscopy analysis (×100 magnification). (D) Apoptotic cell death in KM12, Caco-2 and CCD 841 CoN cells was quantified using Annexin V/7-AAD flow cytometry at 72 hours following treatment. (E) Caspase activities in KM12 and Caco-2 cells were assessed by Caspase Glo^® assay at 72 hours following treatment. (F) 10μM Cud C induced mitochondrial membrane depolarization. Caco-2 and KM12 cells stained with JC-1 at 72 hours after treatment with Cud C. The green dye represents JC-1 monomers in cytoplasm while the red dye represents JC-1 aggregates in nucleus. Cells were observed under fluorescence microscope (×100 magnification). All data represent the mean ± s.d. from at least three independent experiments. Symbol “*” presents the statistical significance concluded from Student’s independent <i>t</i>-test with p-value ≤0.05.</p

IC₅₀ of Cud C and 5-fluorouracil in colorectal cancer and non-transformed colon epithelial cells.

<p>IC₅₀ of Cud C and 5-fluorouracil in colorectal cancer and non-transformed colon epithelial cells.</p

Differential gene expression regulated by cudraflavone C in Caco-2 cells.

<p>(A) Heatmaps generated based on the genes regulated by Cud C. Caco-2 cells were exposed to 10 μM Cud C for 48 hours. GeneChip^® Human Transcriptome Array 2.0 (Affymetrix, USA) was applied. Gene expression changes that ≥2-fold were considered significant. Control 1 and Control 2 represent gene expression from cells treated with vehicle control (1% DMSO); Cud C 1 and Cud C 2 were gene expression from cells treated with Cud C (10 μM). (B) qPCR was used to validate the microarray data. Caco-2 cells were exposed to 10 μM Cud C for 12, 24, 48 or 72 hours The left and right panels present genes that are up and down-regulated respectively. All data represent the mean ± s.d. from at least three independent experiments. Symbol “*” indicates the statistical significance concluded from Student’s independent <i>t</i>-test with p-value ≤0.05.</p