Evidence map›Paper›PMID 32578856›Full record

ArticleBioscience reports2020

NLRP3 augmented resistance to gemcitabine in triple-negative breast cancer cells via EMT/IL-1β/Wnt/β-catenin signaling pathway.

Qiao Zheng, Dejiao Yao, Yi Cai, Tiecheng Zhou

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

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025
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  5. Article
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  9. Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024
    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

4 authors at 1 institution in 1 country.

Qiao ZhengDepartment of Oncology, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine. No. 39 Twelve Bridges Road, Jinniu District, Chengdu 610072, China.
Dejiao YaoDepartment of Oncology, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine. No. 39 Twelve Bridges Road, Jinniu District, Chengdu 610072, China.
Yi CaiDepartment of Oncology, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine. No. 39 Twelve Bridges Road, Jinniu District, Chengdu 610072, China.
Tiecheng ZhouDepartment of Oncology, Sichuan Integrative Medicine Hospital. No. 51, Fourth Section of Renmin South Road, Chengdu 610041, China.
Chengdu University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGemcitabine is widely used in the treatment of breast cancer (BC). However, the resistance to drugs remains a tough concern. The study explored the potential mechanism concerning gemcitabine resistance in triple-negative BC (TNBC) in vitro.

methodsTNBC cells (TNBCC) and gemcitabine-resistance cell lines (GRC) were used. We investigated the sensitivity to gemcitabine responsive to regulation of Nod-like receptor protein 3 (NLRP3) expression in TNBCC in different gemcitabine concentrations. RT-PCR checked NLRP3 mRNA expression and MTT assessed the cell cytotoxicity. Gemcitabine resistance was studied in GRC exposed to 0, 1, 3, 5 nm gemcitabine after GRC were treated with NLRP3 agonist Nigericin sodium salt (NSS) or antagonist CY-09. Epithelial-to-mesenchymal transition (EMT) biomarkers were evaluated via RT-PCR and inflammasome IL-1β, β-catenin content and GSK-3β activity were measured by ELISA methods. Last, we inactivated the signaling and examined the NLRP3, EMT mRNA expression by RT-PCR, IL-1β, β-catenin content and GSK-3β activity by ELISA and cell cytotoxicity through MTT.

resultsNLRP3 up-regulation improved cell survival and reduced sensitivity to gemcitabine (P<0.05). NLRP3 had higher expression in GRC than TNBCC. GRC cell viability dropped as the gemcitabine concentration increased. NLRP3 up-regulation added to resistance to gemcitabine in GRC (P<0.05). NLRP3 agonist might induce EMT process, activate wnt/β-catenin signaling and IL-1β, while inactivation of wnt/β-catenin signaling could result in the inhibition of NLRP3, IL-1β and EMT as well as cell viability in GRC (P<0.05).

conclusionNLRP3 could enhance resistance to gemcitabine via IL-1β/EMT/Wnt/β-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.

Indexed as

Cell Line, TumorDeoxycytidineDose-Response Relationship, DrugDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGemcitabineGene Expression Regulation, NeoplasticHumansInflammasomesInterleukin-1betaNigericinNLR Family, Pyrin Domain-Containing 3 ProteinThiazolidinesThionesTriple Negative Breast NeoplasmsCY-09 compoundDeoxycytidineGemcitabineIL1B protein, humanInflammasomesInterleukin-1betaNigericinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanThiazolidinesThionesgemcitabineIL-1βNLRP3resistanceWnt/β-catenin

Identifiers

PMID32578856
PMCPMC7335831
OpenAlexW3038099274

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.