Evidence map›Paper›PMID 38465429›Full record

ArticleAnti-cancer agents in medicinal chemistry2024

Tabersonine Induces the Apoptosis of Human Hepatocellular Carcinoma

Xuan Li, Xudan Li, Lianghua Chen, Yuan Deng, Zhizhong Zheng, Yanlin Ming

Abstract read
In one paragraph

Article in Anti-cancer agents in medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Piperine and Tabersonine, but Not Lupinine, InhibitInternational journal of molecular sciences · 2025
    Article
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Xuan LiDepartment of Bioengineering and Biotechnology, Institute of Chemical Engineering, Huaqiao University, Xiamen, Fujian, 361021, China.
Xudan LiFujian Provincial Key Laboratory of new target drugs (Xiamen University), School of Pharmaceutical Sciences, Xiamen University, Xiamen, 361021, China.
Lianghua ChenKey Laboratory of Fujian Province for Physiology and Biochemistry of Subtropical Plant, Fujian Institute of Subtropical Botany, Xiamen, 361006, China.
Yuan DengKey Laboratory of Fujian Province for Physiology and Biochemistry of Subtropical Plant, Fujian Institute of Subtropical Botany, Xiamen, 361006, China.
Zhizhong ZhengCollege of Life and Health Sciences, Fuzhou Institute of Technology, Fuzhou, 350506, China.
Yanlin MingDepartment of Bioengineering and Biotechnology, Institute of Chemical Engineering, Huaqiao University, Xiamen, Fujian, 361021, China.

Funding

Traditional Chinese Medicine major science and technology projects of Xiamen of Fujian Province of China 3502Z20211006
6 · The paper itself

Abstract

backgroundTabersonine, 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.

objectiveThe present study aims to investigate the anti-tumor effects of tabersonine and its mechanisms in inducing apoptosis in hepatocellular carcinoma.

methodsThe 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 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.

conclusionOur 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.

Indexed as

ApoptosisCarcinoma, HepatocellularCell ProliferationCell SurvivalDrug Screening Assays, AntitumorIndole AlkaloidsLiver NeoplasmsAnimalsAntineoplastic AgentsAntineoplastic Agents, PhytogenicDose-Response Relationship, DrugHep G2 CellsHumansMembrane Potential, MitochondrialMiceMice, Inbred BALB CAntineoplastic AgentsAntineoplastic Agents, PhytogenicIndole Alkaloidsanti-tumorapoptosisdeath receptor apoptotic pathway.hepatocellular carcinomamitochondrial pathwayTabesonine

Identifiers

PMID38465429
PMCPMC11327752

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.