Evidence map›Paper›PMID 34732786›Full record

ArticleScientific reports2021

The chemotherapeutic drug carboplatin affects macrophage responses to LPS and LPS tolerance via epigenetic modifications.

Atsadang Boonmee, Salisa Benjaskulluecha, Patipark Kueanjinda, Benjawan Wongprom, Thitiporn Pattarakankul, Tanapat Palaga

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. SUV39H1 is a prognosis and immune microenvironment-related biomarker in diffuse large B-cell lymphoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
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  9. Review
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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 1 institution in 1 country.

Atsadang BoonmeeDepartment of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand.
Salisa BenjaskulluechaCenter of Excellence in Immunology and Immune-Mediated Diseases, Chulalongkorn University, Bangkok, Thailand.
Patipark KueanjindaCenter of Excellence in Immunology and Immune-Mediated Diseases, Chulalongkorn University, Bangkok, Thailand.
Benjawan WongpromDepartment of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand.
Thitiporn PattarakankulDepartment of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand.
Tanapat PalagaDepartment of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand. tanapat.p@chula.ac.th.
Chulalongkorn University · TH

Funding

Chulalongkorn University Ratchadaphisek Somphoch Endowment Fund from Chulalongkorn University (760001-HR)Program Management Unit for Human Resources & Institutional Development, Research and Innovation CU B16F630071
6 · The paper itself

Abstract

Following re-exposure to lipopolysaccharide (LPS), macrophages exhibit an immunosuppressive state known as LPS tolerance, which is characterized by repressed proinflammatory cytokine production. LPS-induced tolerance in macrophages is mediated in part by epigenetic changes. Carboplatin, an anticancer chemotherapeutic drug, exerts its effect by inhibiting DNA replication and transcription, as well as through epigenetic modifications. Through an unbiased screen, we found that carboplatin rescued TNF-α and IL-6 production in LPS-tolerant macrophages. Transcriptomic analysis and gene set enrichment analyses revealed that p53 was one of the most significantly upregulated hallmarks in both LPS-primed and LPS-tolerant macrophages in the presence of carboplatin, while E2F and G2/M were the most negatively regulated hallmarks. Heterochromatin protein 1 (HP1-α), which is associated with gene silencing, was significantly reduced in carboplatin-treated LPS-tolerant macrophages at the mRNA and protein levels. Dynamic changes in the mRNA level of genes encoding H3K9me3 methyltransferases, setdb2, kdm4d, and suv39h1 were induced in the presence of carboplatin in LPS-tolerant macrophages. Taken together, we provide evidence that carboplatin treatment interferes with proinflammatory cytokine production during the acute LPS response and LPS tolerance in macrophages, possibly via H3K9me3 modification.

Indexed as

Drug Screening Assays, AntitumorEpigenesis, GeneticAnimalsAntineoplastic AgentsBone Marrow CellsCarboplatinCells, CulturedDrug DesignDrug DiscoveryDrug ToleranceFemaleImmune SystemImmune ToleranceInflammationInterleukin-6LipopolysaccharidesAntineoplastic AgentsCarboplatinInterleukin-6LipopolysaccharidesTranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID34732786
PMCPMC8566489
OpenAlexW3209239609

What OpenQuestion holds

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LicenceCC BY
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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.