In vitro evidence supports cell cycle arrest by alkyl-phospholipid erufosine in pancreatic cancer cell line

Abstract

Background: Pancreatic cancer is an aggressive malignancy with limited therapeutic options and poor prognosis. Dysregulation of cell cycle control is a hallmark of tumor progression, making cell cycle–targeted therapies an attractive strategy. Erufosine, a synthetic alkyl phosphocholine, has shown promising antitumor activity in various cancer models by interfering with signaling pathways involved in cell survival and proliferation. However, its effects on cell cycle regulation in pancreatic cancer cells require investigation.

Methods: Human pancreatic cancer cells were treated with erufosine at defined concentrations for specified time interval. Cell cycle distribution was analyzed using propidium iodide-based staining of DNA followed by flow cytometry. The staining enabled quantification of DNA content to assess proportion of cells in different phases of the cell cycle.

Results: Erufosine treatment resulted in alteration of cell cycle progression in pancreatic cancer cells. Flow cytometric analysis revealed an accumulation of cells in a specific phase of the cell cycle (G2/M), indicating a halt in cell cycle progression compared to untreated controls. This arrest was accompanied by a corresponding reduction in the proportion of cells undergoing active proliferation.

Conclusion: These findings suggest that erufosine exerts its anti-tumor effects in pancreatic cancer, at least in part, by inducing cell cycle arrest. Erufosine may therefore represent a potential therapeutic agent targeting cell cycle dysregulation in pancreatic cancer.