Citalopram enhances cisplatin-induced cytotoxicity in T24 bladder cancer cells: An in vitro study

Citalopram, a potent selective serotonin reuptake inhibitor, has demonstrated potential anticancer effects by triggering apoptosis and inhibiting cell proliferation and metastasis. This study explores how combining citalopram with cisplatin could affect bladder cancer cell proliferation, migration, and apoptosis.

T24 cells were treated with varying concentrations of cisplatin and citalopram using the MTT assay. Cellular migration was assessed using the wound-healing assay. Colony formation was evaluated using the colony-forming assay (CFA). Apoptosis, necrosis, and cell cycle alterations were analyzed by flow cytometry. Quantitative PCR (qPCR) was used to measure the mRNA expression of BAX, BCL2, E-cadherin, N-cadherin, VEGF-C, SNAI1, MMP2, MMP9, and GLUT1.

Cisplatin reduced T24 cell viability in a concentration-dependent manner. The CFA results demonstrated that combining the two agents reduced T24 cell proliferation more effectively than cisplatin alone (p < 0.01), and this effect is associated with a significant decrease in VEGF-C expression in the combination group (p < 0.01). The combination therapy led to a significantly higher rate of apoptosis (P < 0.01) and cell cycle arrest in the G2/M phase (P < 0.001) compared with cells treated with cisplatin alone, associated with a significant increase in the BAX/BCL2 ratio (P < 0.01) alongside a significant decrease in GLUT1 levels (P < 0.0001) observed in the combination therapy. Additionally, the GLUT1 protein level significantly decreased in the combination group compared with cisplatin monotherapy (P < 0.001).

Citalopram has been shown to improve the efficacy of cisplatin in suppressing T24 bladder cancer cells in vitro.