Evidence map›Paper›PMID 26191230›Full record

ArticleInternational journal of clinical and experimental pathology2015

Bevacizumab induces A549 cell apoptosis through the mechanism of endoplasmic reticulum stress in vitro.

Li-Le Wang, Rui-Cheng Hu, Ai-Guo Dai, Shuang-Xiang Tan

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Exploring the efficacy of a novel cannabidiol and bevacizumab combination in non-small cell lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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  8. Clinical development of targeted and immune based anti-cancer therapies.Journal of experimental & clinical cancer research : CR · 2019
    Review
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  10. Article
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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

4 authors at 1 institution in 1 country.

Li-Le WangDepartment of Respiratory Medicine, Hunan Province Geriatric Hospital Changsha 410016, China ; Institute of Respiratory Disease, Hunan Province Geriatric Hospital Changsha 410016, China.
Rui-Cheng HuDepartment of Respiratory Medicine, Hunan Province Geriatric Hospital Changsha 410016, China ; Institute of Respiratory Disease, Hunan Province Geriatric Hospital Changsha 410016, China.
Ai-Guo DaiDepartment of Respiratory Medicine, Hunan Province Geriatric Hospital Changsha 410016, China ; Institute of Respiratory Disease, Hunan Province Geriatric Hospital Changsha 410016, China.
Shuang-Xiang TanDepartment of Respiratory Medicine, Hunan Province Geriatric Hospital Changsha 410016, China ; Institute of Respiratory Disease, Hunan Province Geriatric Hospital Changsha 410016, China.
Hunan Mawangdui Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo observe the effect of bevacizumab on human A549 cells and explore its mechanism.

methodsAfter different concentrations (0 μM, 1 μM, 5 μM, 25 μM) of bevacizumab treating in A549 cells, CCK8 assay detect the impact of bevacizumab on A549 cell proliferation and flow cytometry determine the effect of bevacizumab on human A549 cells apoptosis. Real-time PCR and Western blotting detect the changing expression of the target gene (CHOP, caspase-4, IRE1, XBP-1) on mRNA and Protein level.

resultsTreatment with bevacizumab for 24-hr have induced cell death in a does-dependent manner dramatically (P<0.05). In terms of the mRNA level, expression of XBP-1 has increased obviously in each group (1 μM, 5 μM, 25 μM) (P<0.01); the expression of CHOP (25 μM) and caspase-4 (5 μM) have increased slightly (P<0.05). In terms of the protein level, the expression of CHOP has increased obviously in each group (1 μM, 5 μM, 25 μM) when compared with the control group (0 μM) (P<0.05). As for caspase-4 (5 μM, 25 μM), the expression have increased slightly when compared with the control group (0 μM) (P<0.05).

conclusionBevacizumab can induce A549 cell apoptosis through the mechanism of endoplasmic reticulum stress.

Indexed as

Angiogenesis InhibitorsApoptosisBevacizumabCaspases, InitiatorCell Line, TumorCell ProliferationDNA-Binding ProteinsDose-Response Relationship, DrugEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesGene Expression Regulation, NeoplasticHumansLung NeoplasmsProtein Serine-Threonine KinasesRegulatory Factor X Transcription FactorsAngiogenesis InhibitorsBevacizumabCASP4 protein, humanCaspases, InitiatorDDIT3 protein, humanDNA-Binding ProteinsEndoribonucleasesERN1 protein, humanProtein Serine-Threonine KinasesRegulatory Factor X Transcription FactorsRNA, MessengerTranscription Factor CHOPTranscription FactorsX-Box Binding Protein 1XBP1 protein, humanA549 cellapoptosisBevacizumabendoplasmic reticulum stress

Identifiers

PMID26191230
PMCPMC4503101
OpenAlexW1012659431

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.