Synergistic effects and mechanisms of impressic acid or acankoreanogein in combination with docetaxel on prostate cancer.

Prostate cancer (PCa) is a common cancer among males and a leading cause of cancer deaths. Docetaxel (DOC) was recommended in guidelines as the first first-line drug of PCa; however, treatment with high doses of DOC ultimately results in resistance. This study examined the proliferation, viability, and apoptosis of VCaP cells evaluated by the MTT assay, trypan blue exclusion assay, and morphological assessments to investigate the effects and mechanisms of action by impressic acid (E12-1) or acankoreanogein (E13-1), isolated from (L.) Merr., in combination with DOC in VCaP PCa cells. The research, which also contained cell migration, was examined under a light microscope. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity was assessed by the luciferase reporter assay. Finally, the expression of B-cell lymphoma 2 (Bcl-2), NF-κB, phosphorylated Akt (p-Akt), phosphorylated signal transducer and activator of transcription 3 (p-Stat 3), phosphorylated c-Jun N-terminal kinase (p-JNK), and extracellular signal-related protein kinases 1 and 2 in VCaP cells was evaluated by western blotting. The result is combination of DOC with E12-1 or E13-1 which synergistically inhibited growth, induced apoptosis, and reduced migration of VCaP cells compared with treatment with DOC, E12-1, or E13-1 alone. The potential molecular mechanisms were related to significant decreases in the expression of NF-κB, Bcl-2, p-Stat 3, p-JNK, and p-Akt in VCaP cells. DOC combined with E12-1 or E13-1 may be an effective approach for inhibiting the growth and apoptosis of PCa cells, thus making it possible to reduce the dose of DOC in patients with PCa who experience systemic toxicity.