Erianin Suppresses Pancreatic Cancer Progression by Inducing Cell Cycle Arrest and Ferroptosis

Background: Pancreatic Cancer is a highly aggressive malignancy with limited therapeutic options and poor prognosis. Erianin, a natural product, has shown anti-cancer properties in various malignancies, but its effects on pancreatic Cancer and the underlying mechanisms remain poorly understood.

Aim: This study aimed to evaluate the anti-tumor effects of erianin on pancreatic Cancer cells and to explore the regulatory mechanisms involved.

Methods: PANC-1 and ASPC-1 pancreatic Cancer cells were treated with erianin at different concentrations. Cell viability and proliferation were assessed using the Cell Counting Kit-8 (CCK-8) assay and colony formation assay. Cell cycle distribution was analyzed by flow cytometry. Ferroptosis was evaluated by measuring levels of Fe²⁺, total iron, and lipid Reactive Oxygen Species (ROS). Western blotting was used to detect</mark> the expression of cell cycle regulators and ferroptosis-related proteins.

Results: Erianin significantly suppressed pancreatic Cancer cell viability and proliferation in a dose-dependent manner. It induced G0/G1 phase arrest, accompanied by downregulation of cyclin D1 and cyclin A. Furthermore, erianin promoted Ferroptosis, as evidenced by increased Fe²⁺, total iron, and lipid ROS levels, along with reduced Glutathione Peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression. The Ferroptosis inhibitor Ferrostatin-1 reversed these effects, validating Ferroptosis as a critical mechanism in erianin's anti-cancer activity.

Conclusion: Erianin exerts potent anti-tumor effects on pancreatic Cancer cells by inducing cell cycle arrest and Ferroptosis. These findings establish erianin as a promising therapeutic candidate for pancreatic Cancer treatment.

cell cycle; erianin; ferroptosis; pancreatic cancer.