Brucine Inhibits Proliferation of Pancreatic Ductal Adenocarcinoma through PI3K/AKT Pathway-induced Mitochondrial Apoptosis

Title:Brucine Inhibits Proliferation of Pancreatic Ductal Adenocarcinoma through PI3K/AKT Pathway-induced Mitochondrial Apoptosis

Volume: 24 Issue: 7

Author(s): You Wu, Fenglin Zhang, Panling Xu and Ping Li*

Affiliation:

• Oncology Department of Integrated Traditional Chinese and Western Medicine, The First Affiliated Hospital of Anhui Medical University, 230022, Hefei, Anhui, China
• Department of Integrated Traditional Chinese and Western Medicine, Anhui Medical University, 230022, Hefei, Anhui, China

Keywords: Pancreatic ductal adenocarcinoma, brucine, apoptosis, PI3K/ AKT, mitochondria membrane potential, apoptotic- prone cell population.

Abstract:

Introduction: The purpose of this research was to settle the role of brucine in pancreatic ductal adenocarcinoma (PDAC) and the mechanisms involved.

Methods: The findings of this study suggest that brucine exerts inhibitory effects on cell growth, clonogenicity, and invasive potential of Panc02 and Mia Paca-2 cells. These effects may be linked to an increase in apoptotic-prone cell population.

Results: Gene sequencing data suggests that these effects are mediated through the induction of apoptosis. Experimental evidence further supports the notion that brucine reduces mitochondrial membrane potential and upregulates Bax expression while downregulating Bcl-2 expression. These effects are believed to be a result of brucine-mediated suppression of PI3K/Akt activity, which serves as a regulatory factor of mTOR, Bax, and Bcl-2. Suppression of PI3K activity enhances the tumor-suppressing effects of brucine.

Conclusion: Overall, these findings suggest that brucine has therapeutic potential as a remedy option for PDAC.

Cite this article as:

Wu You, Zhang Fenglin, Xu Panling and Li Ping*, Brucine Inhibits Proliferation of Pancreatic Ductal Adenocarcinoma through PI3K/AKT Pathway-induced Mitochondrial Apoptosis, Current Cancer Drug Targets 2024; 24 (7) . https://dx.doi.org/10.2174/0115680096274284231116104554