Objective: To explore the effect of tanshinone on the invasion of PCa cells induced by androgen-deprivation therapy (ADT) and its possible action mechanism.
Methods: We treated human PCa LNCaP cells with tanshinone at 0 nmol/L (the control group), 5 nmol/L (tanshinone group 1), 10 nmol/L (tanshinone group 2) and 20 nmol/L (tanshinone group 3), respectively. Then we detected their cloning, angiogenesis and invasion abilities by plate cloning assay, tube-formation assay and Transwell chamber assay, respectively, examined their apoptosis using the AnnexinV-FITC/PI double staining method, and determined the protein expressions of phosphatidylinositol 3-kinase (PI3K), p-PI3K, protein kinase B (AKT) and p-AKT by Western blot.
Results: Compared with the control group, the PCa LNCaP cells in the tanshinone groups 1, 2 and 3 showed significant dose-dependent decreases in the clone formation rate (［25.14 ± 5.19］% vs ［19.33 ± 4.12］% vs ［14.69 ± 4.71］% vs ［9.35 ± 2.37］%, P<0.05), number of cellular lumens (［23.20 ± 4.85］ vs ［19.80 ± 5.12］ vs ［14.40 ± 4.16］ vs ［10.20 ± 3.21］ per microscopic field, P<0.05) and count of transmembrane cells (［62.80 ± 8.97］ vs ［50.40 ± 7.62］ vs ［38.60 ± 5.16］ vs ［27.40 ± 4.91］ per microscopic field, P<0.05), increase in the rate of cell apoptosis (［3.58 ± 0.74］% vs ［8.97 ± 1.36］% vs ［14.64 ± 4.10］% vs ［21.17 ± 5.37］%, P<0.05), and down-regulation of the expressions of p-PI3K, PI3K, p-AKT and AKT (P<0.05).
Conclusion: Tanshinone can reverse ADT-induced invasion of PCa cells, reduce their clone formation and angiogenesis, promote their apoptosis, and inhibit the activity of PI3K and AKT signaling pathways.
Keywords: androgen-deprivation therapy; prostate cancer; tanshinone; invasion.