Evidence map›Paper›PMID 33925516›Full record

ArticleCancers2021

Increased Extracellular Adenosine in Radiotherapy-Resistant Breast Cancer Cells Enhances Tumor Progression through A2AR-Akt-β-Catenin Signaling.

Hana Jin, Jong-Sil Lee, Dong-Chul Kim, Young-Shin Ko, Gyeong-Won Lee, Hye-Jung Kim

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Insights from Clinical Trials on AACS pharmacology & translational science · 2025
    Review
  6. Review
  7. Review
  8. Adenosine receptors in breast cancer.Molecular biology reports · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. CD73: Friend or Foe in Lung Injury.International journal of molecular sciences · 2023
    Review
  13. P2YCancers · 2022
    Article
  14. Emerging roles of purinergic signaling in anti-cancer therapy resistance.Frontiers in cell and developmental biology · 2022
    Review
  15. Review
  16. Review
  17. Review
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 2 institutions in 1 country.

Hana JinDepartment of Pharmacology, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea.
Jong-Sil LeeDepartment of Pathology, College of Medicine, Institute of Health Sciences, Gyeongsang National University Hospital, Gyeongsang National University, Jinju 52727, Korea.
Dong-Chul KimDepartment of Pathology, College of Medicine, Institute of Health Sciences, Gyeongsang National University Hospital, Gyeongsang National University, Jinju 52727, Korea.
Young-Shin KoDepartment of Pharmacology, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea.
Gyeong-Won LeeDivision of Hematology-Oncology, Department of Internal Medicine, College of Medicine, Institute of Health Sciences, Gyeongsang National University Hospital, Gyeongsang National University Jinju, Jinju 52727, Korea.
Hye-Jung KimDepartment of Pharmacology, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea.ORCID 0000-0002-7067-6810
Gyeongsang National University · KRGyeongsang National University Hospital · KR

Funding

National Research Foundation of Korea 2018R1A2B6001786National Research Foundation of Korea 2021R1A2B5B0100144611
6 · The paper itself

Abstract

Recently, we found that the expressions of adenosine (ADO) receptors A2AR and A2BR and the ectonucleotidase CD73 which is needed for the conversion of adenosine triphosphate (ATP) to adenosine diphosphate (ADP) and the extracellular ADO level are increased in TNBC MDA-MB-231 cells and RT-R-MDA-MB-231 cells compared to normal cells or non-TNBC cells. The expression of A2AR, but not A2BR, is significantly upregulated in breast cancer tissues, especially TNBC tissues, compared to normal epithelial tissues. Therefore, we further investigated the role of ADO-activated A2AR and its signaling pathway in the progression of RT-R-TNBC. ADO treatment induced MDA-MB-231 cell proliferation, colony formation, and invasion, which were enhanced in RT-R-MDA-MB-231 cells in an A2AR-dependent manner. A2AR activation by ADO induced AKT phosphorylation and then β-catenin, Snail, and vimentin expression, and these effects were abolished by A2AR-siRNA transfection. In an in vivo animal study, compared to 4T1-injected mice, RT-R-4T1-injected mice exhibited significantly increased tumor growth and lung metastasis, which were decreased by A2AR-knockdown. The upregulation of phospho-AKT, β-catenin, Snail, and vimentin expression in mice injected with RT-R-4T1 cells was also attenuated in mice injected with RT-R-4T1-A2AR-shRNA cells. These results suggest that A2AR is significantly upregulated in BC tissues, especially TNBC tissues, and ADO-mediated A2AR activation is involved in RT-R-TNBC invasion and metastasis through the AKT-β-catenin pathway.

Indexed as

A2ARadenosineAktradiotherapy-resistant breast cancer cellsβ-catenin

Identifiers

PMID33925516
PMCPMC8123845
OpenAlexW3158627227

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.