Panoply™ Human CDH2 Over-expressing Stable Cell Line

Enzalutamide is a treatment option for patients with castration-resistant or metastatic prostate cancer. However, a significant proportion of patients develop resistance after a period of enzalutamide treatment. Cells in these tumors often exhibit enhanced proliferation and migration, with N-cadherin (CDH2) appearing to play a key role. Here, researchers investigated the potential effects of CDH2 on the prostate cancer cell line LNCaP by upregulating and downregulating CDH2 expression. Androgen-sensitive LNCaP cells, designated LNCaP enzalutamide-resistant (EnzaR) cells, were treated with 10 µM enzalutamide. The study found increased CDH2 expression in LNCaP EnzaR cells compared to LNCaP cells. Overexpression of CDH2 enhanced cell viability and migration in both LNCaP and LNCaP EnzaR cell lines. Conversely, inhibition of CDH2 expression exhibited the opposite effect. CDH2 expression was also highly correlated with the expression of four epithelial-mesenchymal transition markers, as confirmed by Western blotting. These results suggest that inhibition of CDH2 expression by siRNA transfection significantly affects the physiology of LNCaP EnzaR cells and may represent a potential therapeutic option for prostate cancer.

MTT assay results showed that cell viability in the CDH2-overexpressing LNCaP cell line was higher than in the other two control groups (Figure 1). Similar results were observed in the LNCaP EnzaR cell line (Figure 1A). Next, cell viability in the LNCaP and LNCaP EnzaR cell lines was assessed using the CCK-8 assay. Twenty-four hours after transfection, cell viability in the CDH2-overexpressing LNCaP and LNCaP EnzaR cell lines was also higher than in the other two control groups (Figure 1B). These results indicate that CDH2 overexpression can enhance PCa cell viability.

Figure 1. Overexpression of CDH2 increases LNCaP and LNCaP EnzaR cell viability. (Lu C H, et al., 2022)