Calcium channel blocker (Fendiline) induces cell cycle arrest in pancreatic cancer cells

Abstract

Background: Pancreatic ductal adenocarcinoma is one of the most lethal malignancies worldwide, characterized by late diagnosis, aggressive progression, and resistance to conventional therapies. The urgent need for novel therapeutic strategies has prompted investigation into drug repurposing approach. Fendiline, a non-selective calcium channel blocker with reported anti-proliferative properties, has emerged as a potential candidate. This study aimed to evaluate its impact on cell cycle progression using flow cytometry.

Methods: Human pancreatic cancer cell line (BxPC-3) was treated with increasing concentrations of fendiline (5, 10, 15µM) for the defined time interval (48h). Cell cycle distribution was analyzed by propidium iodide staining followed by flow cytometric quantification of DNA content. Percentage of cells in different phases of the cell cycle were resented in comparison to untreated control.

Results: Compared with untreated control cells, fendiline treatment exhibited a marked increase in the G0/G1 population. At the same time, a concomitant reduction in the S phase fraction in response to exposure with drug was noticed. Quantitative analysis demonstrated a dose-dependent effect, with lower concentrations of fendiline producing a moderate increase in G0/G1 phase cells (49.2%), while higher concentrations resulted in pronounced G1 accumulation (73.2%) as compared to control cell fraction (43.2%).

Conclusion: These findings demonstrate that fendiline exerts anti-proliferative effects in pancreatic cancer cells by disrupting cell cycle progression. Study supports further investigation of fendiline as a repurposed therapeutic cytostatic agent for pancreatic cancer and provides mechanistic insight into its anti-tumor activity.