Evidence map›Paper›PMID 28762597›Full record

ArticleCell proliferation2017

Visfatin mediates doxorubicin resistance in human non-small-cell lung cancer via Akt-mediated up-regulation of ABCC1.

Zhili Cao, Naixin Liang, Huaxia Yang, Shanqing Li

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 24 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

4 authors at 1 institution in 1 country.

Zhili CaoDepartment of Thoracic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100730, China.
Naixin LiangDepartment of Thoracic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100730, China.ORCID http://orcid.org/0000-0002-6320-193X
Huaxia YangDepartment of Rheumatology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100730, China.
Shanqing LiDepartment of Thoracic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100730, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesNon-small-cell lung cancer (NSCLC) is one of the leading causes of cancer deaths worldwide. Increasing levels of visfatin are correlated with worse clinical prognosis of NSCLC. However, the effects of visfatin on drug resistant are still not well illustrated. MATERIALS AND

methodsEffects of visfatin on drug resistant cells were checked by CCK-8 kit. Gene and protein variations were measured by real-time PCR and western blot analysis, respectively.

resultsOur present data confirmed that expression of visfatin was significantly increased in NSCLC cells and tissues. In addition, protein and mRNA expression of visfatin were significantly elevated in doxorubicin (Dox) resistance of NSCLC cells when compared with their corresponding sensitivity parental cells. Overexpression of visfatin can down-regulate the Dox sensitivity of NSCLC cells and up-regulate the mRNA and protein expression of ABCC1, while has no effect on ABCB1. Knockdown of visfatin can down-regulate the expression of ABCC1 in Dox-resistant NSCLC cells. Visfatin can increase the phosphorylation and nuclear localization of Akt in NSCLC cells. LY294002 can decrease the expression of multidrug resistance protein-1 (MRP1) in NSCLC Dox-resistant cells. Chromatin immunoprecipitation assays showed that overexpression of visfatin can significantly increase the binding of Akt with the promoter of ABCC1 in both A549 and H1793 cells.

conclusionsThese data showed that visfatin can decrease Dox sensitivity of NSCLC cells via activation of Akt/MRP1. It indicated that inhibition of visfatin signals might be a promising therapeutic strategy for the management of chemoresistance of NSCLC patients.

Indexed as

Antibiotics, AntineoplasticATP-Binding Cassette, Sub-Family C ProteinsCarcinoma, Non-Small-Cell LungCell Line, TumorDoxorubicinDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansLungLung NeoplasmsNicotinamide PhosphoribosyltransferaseProto-Oncogene Proteins c-aktAntibiotics, AntineoplasticATP-Binding Cassette, Sub-Family C ProteinsDoxorubicinmultidrug resistance-associated protein 1Nicotinamide PhosphoribosyltransferaseProto-Oncogene Proteins c-akt

Identifiers

PMID28762597
PMCPMC6529115
OpenAlexW2740071091

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.