Evidence map›Paper›PMID 31182137›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

AKR1C1 controls cisplatin-resistance in head and neck squamous cell carcinoma through cross-talk with the STAT1/3 signaling pathway.

Wei-Min Chang, Yu-Chan Chang, Yi-Chieh Yang, Sze-Kwan Lin, Peter Mu-Hsin Chang, Michael Hsiao

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 72 citations in OpenAlex.

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  20. STAT3 Activation as a Predictive Biomarker for Ruxolitinib Response in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 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

6 authors at 4 institutions in 1 country.

Wei-Min ChangGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Yu-Chan ChangGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Yi-Chieh YangGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Sze-Kwan LinDepartment of Dentistry, National Taiwan University Hospital, Taipei, Taiwan.
Peter Mu-Hsin ChangDepartment of Oncology, Taipei Veterans General Hospital, Taipei, Taiwan. ptchang@vghtpe.gov.tw.
Michael HsiaoGenomics Research Center, Academia Sinica, Taipei, Taiwan. mhsiao@gate.sinica.edu.tw.ORCID http://orcid.org/0000-0001-8529-9213
Genomics Research Center, Academia Sinica · TWKaohsiung Medical University · TWNational Taiwan University Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

Academia Sinica and Ministry of Science and Technology AS-SUMMIT-108Ministry of Science and Technology, Taiwan MOST 107-2627-M-075 -001
6 · The paper itself

Abstract

backgroundCisplatin is the first-line chemotherapy used against most upper aerodigestive tract carcinomas. In head and neck cancer, sensitivity to cisplatin remains the key issue in treatment response and outcome. Genetic heterogeneity and aberrant gene expression may be the intrinsic factors that cause primary cisplatin-resistance.

methodsCombination of the HNSCC gene expression data and the cisplatin sensitivity results from public database. We found that aldo-keto reductase family 1 member C1 (AKR1C1) may be associated with cisplatin sensitivity in HNSCC treatment of naïve cells. We examined the AKR1C1 expression and its correlation with cisplatin IC

resultsAKR1C1 positively correlates to cisplatin-resistance in HNSCC cells. AKR1C1 is a poor prognostic factor for recurrence and death of HNSCC patients. Silencing of AKR1C1 not only reduced in vitro IC

conclusionsAKR1C1 is a crucial regulator for cisplatin-resistance in HNSCC and also poor prognostic marker for patients. Targeting the AKR1C1-STAT axis may provide a new therapeutic strategy to treat patients who are refractory to cisplatin treatment.

Indexed as

Signal Transduction20-Hydroxysteroid DehydrogenasesAnimalsAntineoplastic AgentsApoptosisCaspasesCell Line, TumorCell SurvivalCisplatinDisease Models, AnimalGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInflammation MediatorsMiceModels, Biological20-Hydroxysteroid Dehydrogenases3 alpha-beta, 20 beta-hydroxysteroid dehydrogenaseAntineoplastic AgentsCaspasesCisplatinInflammation MediatorsProtein Kinase InhibitorsSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 Transcription FactorAKR1C1Cisplatin-resistanceHNSCCRuxolitinibSTATs

Identifiers

PMID31182137
PMCPMC6558898
OpenAlexW2953087511

What OpenQuestion holds

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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.