Evidence map›Paper›PMID 28042952›Full record

ArticleOncotarget2017

Uncoupling protein 2 downregulation by hypoxia through repression of peroxisome proliferator-activated receptor γ promotes chemoresistance of non-small cell lung cancer.

Mingxing Wang, Guoyin Li, Zhiwei Yang, Lei Wang, Lei Zhang, Ting Wang, Yimeng Zhang, Shengli Zhang, Yong Han, Lintao Jia

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  3. Differential regulation of mitochondrial uncoupling protein 2 in cancer cells.Biochimica et biophysica acta. Bioenergetics · 2024
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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 2 institutions in 1 country.

Mingxing WangDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Guoyin LiState Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, China.
Zhiwei YangDepartment of Applied Physics, Xi'an Jiaotong University, Xi'an, China.
Lei WangState Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, China.
Lei ZhangDepartment of Applied Physics, Xi'an Jiaotong University, Xi'an, China.
Ting WangState Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, China.
Yimeng ZhangState Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, China.
Shengli ZhangDepartment of Applied Physics, Xi'an Jiaotong University, Xi'an, China.
Yong HanDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Lintao JiaState Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, China.
Air Force Medical University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxic microenvironment is critically involved in the response of non-small cell lung cancer (NSCLC) to chemotherapy, the mechanisms of which remain largely unknown. Here, we found that NSCLC patients exhibited increased chemotherapeutic resistance when complicated by chronic obstructive pulmonary disease (COPD), a critical cause of chronic hypoxemia. The downregulation of uncoupling protein 2 (UCP2), which is attributed to hypoxia-inducible factor 1 (HIF-1)-mediated suppression of the transcriptional factor peroxisome proliferator-activated receptor γ (PPARγ), was involved in NSCLC chemoresistance, and predicted a poor survival rate of patients receiving routine chemotherapy. UCP2 suppression induced reactive oxygen species production and upregulation of the ABC transporter protein ABCG2, which leads to chemoresistance by promoting drug efflux. UCP2 downregulation also altered metabolic rates as shown by elevated glucose uptake and reduced oxygen consumption. These data suggest that UCP2 is a key mediator of hypoxia-triggered chemoresistance of NSCLCs, which can be potentially targeted in clinical treatment of chemo-refractory NSCLCs.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2Carcinoma, Non-Small-Cell LungCell Line, TumorCellular ReprogrammingCisplatinDocetaxelDose-Response Relationship, DrugDown-RegulationEnergy MetabolismGene Expression Regulation, NeoplasticGlucoseHumansLung NeoplasmsNeoplasm ProteinsABCG2 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2CisplatinDocetaxelGlucoseNeoplasm ProteinsPPAR gammaReactive Oxygen SpeciesTaxoidsUCP2 protein, humanUncoupling Protein 2chemotherapeutic resistancehypoxianon-small cell lung cancer (NSCLC)PPAR-γuncoupling protein 2 (UCP2)

Identifiers

PMID28042952
PMCPMC5352384
OpenAlexW2567212964

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.