Evidence map›Paper›PMID 27813328›Full record

ArticleThoracic cancer2017

Depleted aldehyde dehydrogenase 1A1 (ALDH1A1) reverses cisplatin resistance of human lung adenocarcinoma cell A549/DDP.

Yunyan Wei, Shuangshuang Wu, Wei Xu, Yan Liang, Yue Li, Weihong Zhao, Jianqing Wu

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 29 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

7 authors at 2 institutions in 1 country.

Yunyan WeiDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Shuangshuang WuDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wei XuDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yan LiangDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yue LiDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Weihong ZhaoDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jianqing WuDepartment of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCisplatin is the standard first-line chemotherapeutic agent for the treatment of non-small cell lung cancer (NSCLC). However, resistance to chemotherapy has been a major obstacle in the management of NSCLC. Aldehyde dehydrogenase 1A1 (ALDH1A1) overexpression has been observed in a variety of cancers, including lung cancer. The purpose of this study was to investigate the effect of ALDH1A1 expression on cisplatin resistance and explore the mechanism responsible.

methodsReverse transcriptase-PCR was applied to measure the messenger RNA expression of ALDH1A1, while Western blot assay was employed to evaluate the protein expression of ALDH1A1, B-cell lymphoma 2, Bcl-2-like protein 4, phospho-protein kinase B (p-AKT) and AKT. A short hairpin RNA was used to knockdown ALDH1A1 expression. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to determine the effect of ALDH1A1 decrease on cell viability. The cell apoptotic rate was tested using flow cytometry assay.

resultsALDH1A1 is overexpressed in cisplatin resistant cell line A549/DDP, compared with A549. ALDH1A1 depletion significantly decreased A549/DDP proliferation, increased apoptosis, and reduced cisplatin resistance. In addition, the phosphoinositide 3-kinase (PI3K) / AKT pathway is activated in A549/DDP, and ALDH1A1 knockdown reduced the phosphorylation level of AKT. Moreover, the combination of ALDH1A1-short hairpin RNA and PI3K/AKT pathway inhibitor LY294002 markedly inhibited cell viability, enhanced apoptotic cell death, and increased cisplatin sensitivity.

conclusionThese results suggest that ALDH1A1 depletion could reverse cisplatin resistance in human lung cancer cell line A549/DDP, and may act as a potential target for the treatment of lung cancers resistant to cisplatin.

Indexed as

Drug Resistance, NeoplasmAdenocarcinomaAdenocarcinoma of LungAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyApoptosisCell Line, TumorCell ProliferationCell SurvivalCisplatinGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanCisplatinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRetinal DehydrogenaseAldehyde dehydrogenase 1A1apoptosiscisplatin resistancenon-small cell lung cancerproliferation

Identifiers

PMID27813328
PMCPMC5217899
OpenAlexW2555070594

What OpenQuestion holds

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Registered trials

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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.