Effect of Icariin on Androgen Receptor Signaling Pathway in SCID Mice Prostate Cancer Orthotopic Transplantation Tumor

  Objective: To observe the effect of icariin on the androgen receptor signaling pathway of prostate cancer orthotopic transplantation tumor in SCID mice.

  Methods: 64 male SCID mice were randomly divided into model group, experimental group A, group B and group C. The orthotopic transplantation model of prostate cancer was established by intra-prostatic injection of human LNCaP prostate cancer cell line suspension. Experimental group A, group B and group C were given icariin by intragastric administration at doses of 10 mg/kg, 40 mg/kg and 80 mg/kg respectively for 5 weeks after modeling for 2 weeks, and the model group was given normal saline as a control. RT-PCR detection of androgen receptor (AR) and tensin homologous chromosome 10 deletion of phosphatase gene (phosphatase and tensin homolog deleted onchromosometen, PTEN) expression, Western blotting was used to detect prostate cancer-specific antigen (PSA) and phosphorylation AR (p-AR), flow cytometry method to detect the cycle of LNCaP prostate cancer cells.

  Results: AR, p-AR, AR mRNA was highly expressed before and after treatment in the model group, and PTEN mRNA was low. The tumor inhibition rate in the model group was lower. There was no significant difference in tumor mass and tumor volume before and after treatment (P>0.05). In experimental group B and C, the tumor inhibition rate after treatment reached (42.53±5.72)%, (44.81±4.76)%, the two groups had low expression of ARmRNA, p-AR and PSA, high expression of PTENmRNA, and the proportion of cells in G0/G1 phase decreased 、S-phase cell ratio increased, tumor cell proliferation was blocked in S-phase, compared with the model group before treatment, the difference was significant (P<0.05).

  Conclusion: Icariin may inhibit the proliferation of prostate cancer LNCaP cells by inhibiting AR phosphorylation, enhancing PTEN expression and arresting tumor cell proliferation in the S phase.