Evidence map›Paper›PMID 25674005›Full record

ArticleOncoTargets and therapy2015

Tubeimoside-1 induces glioma apoptosis through regulation of Bax/Bcl-2 and the ROS/Cytochrome C/Caspase-3 pathway.

Geng Jia, Qiang Wang, Rong Wang, Danni Deng, Lian Xue, Naiyuan Shao, Yi Zhang, Xiwei Xia, Feng Zhi, Yilin Yang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
25.0field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 89 citations in OpenAlex.

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  11. MicroRNA-34a Promotes Ischemia-Induced Cardiomyocytes Apoptosis through Targeting Notch1.Evidence-based complementary and alternative medicine : eCAM · 2022
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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

10 authors at 1 institution in 1 country.

Geng JiaDepartment of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Qiang WangModern Medical Research Center, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Rong WangModern Medical Research Center, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Danni DengModern Medical Research Center, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Lian XueModern Medical Research Center, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Naiyuan ShaoDepartment of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Yi ZhangDepartment of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Xiwei XiaDepartment of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Feng ZhiModern Medical Research Center, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Yilin YangDepartment of Neurosurgery, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China ; Modern Medical Research Center, Third Affiliated Hospital of Soochow University, Jiangsu, People's Republic of China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTubeimoside-1 (TBMS1) is a natural compound isolated from tubeimoside, which has been widely used as a traditional Chinese herbal medicine. The purpose of the present study is to investigate the anti-tumor effect and the underling mechanism of TBMS1 on glioma cancer cells.

methodsThe MTT assay was performed to evaluate the effect of TBMS1 on glioma cell proliferation. The fluorescent microscopy and flow cytometry analysis were performed to evaluate the effect of TBMS1 on glioma cell apoptosis. The Western blot analysis was used to evaluate the protein change.

resultsTBMS1 inhibited glioma cancer cell proliferation in a dose- and time-dependent manner. Fluorescent microscopy and flow cytometry analysis demonstrated that TBMS1 induced glioma cell apoptosis in a concentration-dependent manner. Western blotting showed that TBMS1 induced apoptosis by increasing the expression of Bax and downregulating the level of Bcl-2. Furthermore, we found that TBMS1 induced apoptosis by increasing the concentration of reactive oxygen species through the release of Cytochrome C and activation of Caspase-3.

conclusionThese findings indicate that TBMS1 may be developed as a possible therapeutic agent for the management of glioma.

Indexed as

apoptosisgliomaproliferationTubeimoside-1

Identifiers

PMID25674005
PMCPMC4321652
OpenAlexW2086668210

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.