Title:Tabersonine Induces the Apoptosis of Human Hepatocellular Carcinoma In vitro and
In vivo
Volume: 24
Issue: 10
Author(s): Xuan Li, Xudan Li, Lianghua Chen, Yuan Deng, Zhizhong Zheng and Yanlin Ming*
Affiliation:
- Department of Bioengineering and Biotechnology, Institute of Chemical Engineering, Huaqiao University, Xiamen, Fujian, 361021,
China
- Key Laboratory of Fujian Province for Physiology and Biochemistry of Subtropical Plant, Fujian
Institute of Subtropical Botany, Xiamen, 361006, China
Keywords:
Tabesonine, anti-tumor, hepatocellular carcinoma, apoptosis, mitochondrial pathway, death receptor apoptotic pathway.
Abstract:
Background: Tabersonine, a natural indole alkaloid derived from Apocynaceae plants, exhibits antiinflammatory
and acetylcholinesterase inhibitory activities, among other pharmacological effects. However, its
anti-tumor properties and the underlying molecular mechanisms remain underexplored.
Objective: The present study aims to investigate the anti-tumor effects of tabersonine and its mechanisms in inducing
apoptosis in hepatocellular carcinoma.
Methods: The inhibitory effects of tabersonine on the viability and proliferation of liver cancer cells were evaluated
using MTT assay and colony formation assay. AO/EB, Hoechst, and Annexin V-FITC/ PI staining techniques
were employed to observe cell damage and apoptosis. JC-1 staining was used to detect changes in mitochondrial
membrane potential. Western blot analysis was conducted to study the anti-tumor mechanism of tabersonine
on liver cancer cells. Additionally, a xenograft model using mice hepatoma HepG2 cells was established
to assess the anti-tumor potency of tabersonine in vivo.
Results and Discussion: Our findings revealed that tabersonine significantly inhibited cell viability and proliferation,
inducing apoptosis in liver cancer cells. Treatment with tabersonine inhibited Akt phosphorylation, reduced
mitochondrial membrane potential, promoted cytochrome c release from mitochondria to the cytoplasm, and
increased the ratio of Bax to Bcl-2. These findings suggested that tabersonine induces apoptosis in liver cancer
cells through the mitochondrial pathway. Furthermore, tabersonine treatment activated the death receptor pathway
of apoptosis. In vivo studies demonstrated that tabersonine significantly inhibited xenograft tumor growth.
Conclusion: Our study is the first to demonstrate that tabersonine induces apoptosis in HepG2 cells through both
mitochondrial and death receptor apoptotic pathways, suggesting its potential as a therapeutic agent candidate for
hepatic cancer.
