Fig. 3: Triptolide reverses cellular resistance to paclitaxel by inhibiting the Hedgehog pathway.

a Box plots showing the distribution of gene expression levels for each group in the sequencing data. b 3D-plot of principal component analysis (PCA) analysis of different treatment groups. c Overlapping DEGs from the three comparisons were shown in the Venn diagram according to the RNA-seq data. d Representative terms from KEGG pathway enrichment analysis based on the overlapping DEGs. e GSEA was performed in KEGG Hedgehog signaling pathway gene sets. f, g RT‒qPCR and Western blotting verified the expression levels of SHH, PTCH1, GLI2, and GLI3 in the indicated cells with or without triptolide treatment. h A549/PR and H460/PR cells were treated with cyclopamine (5 or 10 μM) for 24 h. A CCK-8 assay was applied to quantify cell viability. i Western blotting was used to detect the protein levels of the indicated genes in cyclopamine-treated paclitaxel-resistant cells. j Dose–response curves of paclitaxel in cyclopamine-treated resistant cells were plotted based on CCK-8 assays. Histograms revealed the IC₅₀ value calculated from the fitted curves. Data are indicated as the mean ± SD, **P < 0.01, ***P < 0.001. TPL triptolide, Cyc cyclopamine, PR paclitaxel resistance.