Evidence map›Paper›PMID 26794215›Full record

ArticlePloS one2016

Aspirin Breaks the Crosstalk between 3T3-L1 Adipocytes and 4T1 Breast Cancer Cells by Regulating Cytokine Production.

Chia-Chien Hsieh, Yu-Shan Huang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. BioMedicine · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. The pleiotropic roles of adipocyte secretome in remodeling breast cancer.Journal of experimental & clinical cancer research : CR · 2022
    Review
  7. Review
  8. Cancer-associated adipocytes: emerging supporters in breast cancer.Journal of experimental & clinical cancer research : CR · 2020
    Review
  9. Overcoming cancer therapeutic bottleneck by drug repurposing.Signal transduction and targeted therapy · 2020
    Review
  10. Article
  11. Anti-Inflammatory Drug Use and Ovarian Cancer Risk by COX1/COX2 Expression and Infiltration of Tumor-Associated Macrophages.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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

2 authors at 1 institution in 1 country.

Chia-Chien HsiehDepartment of Human Development and Family Studies, National Taiwan Normal University, Taipei, Taiwan.
Yu-Shan HuangDepartment of Human Development and Family Studies, National Taiwan Normal University, Taipei, Taiwan.
National Taiwan Normal University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is one of the most common cancers in women worldwide. The obesity process is normally accompanied by chronic, low-grade inflammation. Infiltration by inflammatory cytokines and immune cells provides a favorable microenvironment for tumor growth, migration, and metastasis. Epidemiological evidence has shown that aspirin is an effective agent against several types of cancer. The aim of this study is to investigate the anti-inflammatory and anti-cancer effects of aspirin on 3T3-L1 adipocytes, 4T1 murine breast cancer cells, and their crosstalk. The results showed that aspirin treatment inhibited differentiation and lipid accumulation by 3T3-L1 preadipocytes, and decreased the secretion of the inflammatory adipokine MCP-1 after stimulation with tumor necrosis factor (TNF)-α or conditioned medium from RAW264.7 cells. In 4T1 cells, treatment with aspirin decreased cell viability and migration, possibly by suppressing MCP-1 and VEGF secretion. Subsequently, culture of 4T1 cells in 3T3-L1 adipocyte-conditioned medium (Ad-CM) and co-culture of 3T3-L1 and 4T1 cells using a transwell plate were performed to clarify the relationship between these two cell lines. Aspirin exerted its inhibitory effects in the transwell co-culture system, as well as the conditioned-medium model. Aspirin treatment significantly inhibited the proliferation of 4T1 cells, and decreased the production of MCP-1 and PAI-1 in both the Ad-CM model and co-culture system. Aspirin inhibited inflammatory MCP-1 adipokine production by 3T3-L1 adipocytes and the cell growth and migration of 4T1 cells. It also broke the crosstalk between these two cell lines, possibly contributing to its chemopreventive properties in breast cancer. This is the first report that aspirin's chemopreventive activity supports the potential application in auxiliary therapy against obesity-related breast cancer development.

Indexed as

3T3-L1 CellsAdipocytesAnimalsAnti-Inflammatory Agents, Non-SteroidalApoptosisAspirinBreast NeoplasmsCell DifferentiationCell MovementCell ProliferationCells, CulturedChemokine CCL2Coculture TechniquesCulture Media, ConditionedEnzyme-Linked Immunosorbent AssayFemaleAnti-Inflammatory Agents, Non-SteroidalAspirinCCL2 protein, humanChemokine CCL2Culture Media, ConditionedPlasminogen Activator Inhibitor 1SERPINE1 protein, humanVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID26794215
PMCPMC4721678
OpenAlexW2411649082

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.