Evidence map›Paper›PMID 31814899›Full record

ArticleAmerican journal of translational research2019

Betulinic acid induces autophagy-mediated apoptosis through suppression of the PI3K/AKT/mTOR signaling pathway and inhibits hepatocellular carcinoma.

Weiping Liu, Shaoling Li, Ziling Qu, Yi Luo, Ruifeng Chen, Sufen Wei, Xin Yang, Qi Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
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

32 citing papers in PubMed, 47 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Weiping LiuThe First Clinical Medical College, Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Shaoling LiThe Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Ziling QuInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Yi LuoInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Ruifeng ChenThe Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Sufen WeiInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Xin YangDepartment of Pharmacy, The Fifth Affiliated Hospital of Guangzhou Medical University Guangzhou 510700, Guangdong, PR China.
Qi WangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine Guangzhou 510006, Guangdong, PR China.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Betulinic acid (BA) is a pentacyclic triterpenoid compound that widely exists in Chinese herbal medicine, and it has remarkable biological activity. However, the involved molecular targets and mechanisms of BA are still ambiguous. Here, we aim to validate the preventive effects and molecular mechanisms of BA against hepatocellular carcinoma via related experiments. We extracted the 2D and 3D structure of BA from the PubChem database. MTT assay and colony formation assay were used to determine the anti-proliferation and cytotoxicity of BA using in vitro cell models. Hoechst 33258 staining was used to investigate the extent of apoptosis after BA treatment. Western blot and immunofluorescence experiments were used to evaluate apoptosis-related and autophagy-related proteins and molecular mechanisms. We demonstrated that BA significantly inhibited cell proliferation in HepG2 and SMMC-7721 hepatocellular carcinoma cells, but with little cytotoxicity effects on l-02 normal liver cells. We further determined that the hepatocellular carcinoma prevention effects of BA were closely correlated with apoptosis and autophagy. Furthermore, our data indicated that BA-induced autophagy has a protective effect against cancer cell proliferation and promotes cell apoptosis. Additionally, apoptosis and autophagy were induced by BA through suppression of the PI3K/AKT/mTOR signaling pathway. Collectively, our study provides experimental evidence that BA inhibits cell proliferation and induces cell apoptosis and autophagy via suppressing the PI3K/AKT/mTOR pathway. Additionally, BA is a safe and effective herbal medicine compound that can be used for the prevention of hepatocellular carcinoma growth, and may be a potential therapeutic strategy against hepatocellular carcinoma.

Indexed as

autophagy-mediated apoptosisBetulinic acid (BA)hepatocellular carcinomaPI3K/AKT/mTOR

Identifiers

PMID31814899
PMCPMC6895530
OpenAlexW2997349006

What OpenQuestion holds

Textmetadata
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.