To investigate the effects of bicalutamide (BIC) on the malignant biological behavior of prostate cancer LNCaP cells through cadherin 7 (CDH7), and to explore its possible mechanism of action.

This study was divided into two parts, animal experiment and cell experiment. In animal experiment, 30 Balb/c male nude mice were randomly divided into animal blank control group (daily gavage of 10 mL·kg^-1 0.5% carboxymethyl cellulose sodium solution), animal positive control group (daily gavage of 10 mL·kg^-1 enzalutamide) and animal experimental group (daily gavage of 25 mg·kg^-1 BIC), with 10 nude mice in each group. All mice were treated with subcutaneous injection of LNCaP cell suspension to establish a xenograft model and each group was continuously treated for 28 days. The tumor volume of nude mice in each group was recorded every 7 days; tumor tissues were collected 24 h after drug withdrawal; the expression of proliferating cell nuclear antigen (PCNA) protein was detected by immunohistochemistry. In cell experiment, LNCaP cells were divided into cell blank control group (normal culture, no treatment), cell positive control group (treated with enzalutamide 1 μM), cell experimental group (treated with BIC 50 μM), oe-NC group (transfected with oe-NC plasmid and then treated with BIC 50 μM), and oe-CDH7 group (transfected with oe-CDH7 plasmid and then treated with BIC 50 μM). The relative expression levels of CDH7 mRNA in cells was detected by real-time fluorescence quantitative polymerase chain reaction method. The cell invasion ability and apoptosis rate were detected by Transwell assay and terminal-deoxynucleotidyl transferase mediated nick end labeling method, respectively. The activities of superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay. The relative expression levels of CDH7 and proteins related to relevant pathways were detected by Western blot.

In animal experiments, the tumor volume on day 21 of animal blank control group, animal positive control group and animal experimental group were (622.30±131.15), (411.90±72.07) and (467.40±63.92) mm³, respectively; the tumor volumes on day 28 were (1 189.50±225.95), (729.40±142.90) and (688.60±89.07) mm³, respectively; and the relative expression levels of PCNA protein were 1.00±0.11, 0.28±0.09 and 0.33±0.07, respectively. There were statistically significant differences compared animal positive control group or animal experimental group with the control group (all P<0.001). In cell experiments, the relative expression levels of CDH7 mRNA in the cell blank control group, cell positive control group, cell experimental group, oe-NC group and oe-CDH7 group were 1.00±0.16, 0.35±0.07, 0.40±0.05, 0.37±0.05 and 3.12±0.34, respectively; the number of cell invasions were (134.26±24.97), (57.63±11.53), (66.34±11.84), (61.17±9.12) and (98.08±15.88) pieces, respectively; the MDA levels were (126.94±20.81), (257.63±46.19), (239.21±29.32), (244.35±38.46) and (187.79±25.35) pg·mL^-1, respectively; the apoptosis rates were (4.54±0.87)%, (53.27±6.14)%, (47.13±7.15)%, (51.76±9.59)% and (17.49±3.48) %, respectively; the relative expression levels of extracellular signal-regulated kinase 1/2 (ERK1/2) protein were 1.00±0.12, 0.44±0.06, 0.39±0.05, 0.41±0.03 and 0.67±0.11, respectively. Compared cell positive control group, or cell experimental group with cell blank control group, compared oe-CDH7 group with oe-NC group, the above indicators were all statistically significantly different (all P<0.001).

BIC could inhibit the invasion of prostate cancer LNCaP cells and promote their apoptosis through CDH7, and the mechanism of action may be related to the inhibition of mitogen-activated protein kinase (MAPK)-ERK signaling pathway activation.