已发表论文

埃里安素通过诱导细胞周期停滞和铁死亡抑制胰腺癌进展

 

Authors Qu X, He B, Zhang Y, Hang L, Lu P

Received 14 May 2025

Accepted for publication 15 June 2025

Published 15 August 2025 Volume 2025:17 Pages 1657—1666

DOI https://doi.org/10.2147/CMAR.S540437

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Professor Kattesh Katti

Xiao Qu,1 Bin He,2 Yaohui Zhang,1 Li Hang,3 Ping Lu2 

1Department of Gastroenterology, Zhangjiagang Hospital Affiliated to Soochow University, Zhangjiagang, People’s Republic of China; 2Zhangjiagang Hospital Affiliated to Soochow University, Zhangjiagang, People’s Republic of China; 3Department of Gastroenterology, Zhangjiagang Hospital of Traditional Chinese Medicine, Zhangjiagang, People’s Republic of China

Correspondence: Ping Lu, Email pvv671@yeah.net

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 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.

Keywords: erianin, ferroptosis, cell cycle, pancreatic cancer