Lathyrol affects the expression of AR and PSA and inhibits the malignant behavior of RCC cells

To investigate how lathyrol affects aggressive behaviors and related proteins of the androgen receptor (AR) 786-O cells.

786-O cells were cultured in vitro and divided into these groups at random: the dimethylsulfoxide (DMSO) control group (A group), negative control group (B group), and experimental group (C group). Cells in A group were grown in DMSO working medium (contained RPMI 1640 medium and 1% DMSO), B group cells were cultured in nilutamide working medium (contained DMSO working medium and 325 μg/mL nilutamide), while those in C group were cultured in lathyrol working medium (contained DMSO working medium and 300 μg/mL lathyrol). Cell proliferation was measured via CCK-8 assays, and cell apoptosis was examined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Scratch tests and Transwell invasion tests were used to evaluate cell movement and penetration. The expression information about p-AR, AR, p-Akt, ki67, caspase3, cleaved-caspase3, Bcl-2, Bax, caspase9, cleaved-caspase9, and GAPDH proteins was investigated through western blotting. Immunocytochemistry was used to identify the 786-O cells' secretion level of matrix metalloproteinase 2 (MMP2), MMP9, and prostate-specific antigen (PSA) proteins.

The negative control and experimental groups' cells exhibited reduced proliferation, migration, and invasion and increased apoptosis after 24 h treatment. Furthermore, these two group cells exhibited a notable reduction in the status of Ki67, Bcl-2, MMP2, MMP9, and p-Akt (P < 0.05) and significantly increased the expressions of AR, p-AR, Bax, cleaved-caspase3, and cleaved-caspase9 (P < 0.05). There was no statistical distance in PSA, caspase3, and caspase9 expressions among the three groups (P > 0.05).

In vitro, lathyrol and nilutamide exert notable anticancer effects by effectively suppressing the proliferation, migration, and invasion of 786-O cells while also inducing apoptosis.