Evidence map›Paper›PMID 26228921›Full record

ArticleBMC cancer2015

Adenosine A2b receptor promotes progression of human oral cancer.

Hiroki Kasama, Yosuke Sakamoto, Atsushi Kasamatsu, Atsushi Okamoto, Tomoyoshi Koyama, Yasuyuki Minakawa, Katsunori Ogawara, Hidetaka Yokoe, Masashi Shiiba, Hideki Tanzawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 78 citations in OpenAlex.

  1. Adenosine A2B Receptor Promotes Tumor Progression and Metastases in Undifferentiated Pleomorphic Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  9. Adenosine receptors in breast cancer.Molecular biology reports · 2024
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  15. Review
  16. Targeting purine metabolism in ovarian cancer.Journal of ovarian research · 2022
    Review
  17. Generation of a Retargeted OncolyticInternational journal of molecular sciences · 2021
    Article
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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

11 authors at 3 institutions in 1 country.

Hiroki KasamaDepartment of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. porsche_0108@yahoo.co.jp.
Yosuke SakamotoDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. end@faculty.chiba-u.jp.
Atsushi KasamatsuDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. kasamatsua@faculty.chiba-u.jp.
Atsushi OkamotoDepartment of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. onefoot_mactwist@yahoo.co.jp.
Tomoyoshi KoyamaDepartment of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. koyamatomoyo4@gmail.com.
Yasuyuki MinakawaDepartment of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. d02a032d@yahoo.co.jp.
Katsunori OgawaraDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. katsunori.ogawara@faculty.chiba-u.jp.
Hidetaka YokoeDepartment of Oral and Maxillofacial Surgery Research Institute, National Defense Medical College Hospital, 3-2, Namiki, Tokorozawa-shi, Saitama, 359-8513, Japan. yokoe@ndmc.ac.jp.
Masashi ShiibaDepartment of Medical Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. m.shiiba@faculty.chiba-u.jp.
Hideki TanzawaDepartment of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. tanzawap@faculty.chiba-u.jp.
Katsuhiro UzawaDepartment of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. uzawak@faculty.chiba-u.jp.
Chiba University · JPChiba University Hospital · JPNational Defense Medical College Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdenosine A2b receptor (ADORA2B) encodes an adenosine receptor that is a member of the G protein-coupled receptor superfamily. This integral membrane protein stimulates adenylate cyclase activity in the presence of adenosine. Little is known about the relevance of ADORA2B to human malignancy including oral squamous cell carcinoma (OSCC). We aimed to characterize the expression state and function of ADORA2B in OSCC.

methodsThe ADORA2B expression levels in nine OSCC-derived cells were analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses. Using an ADORA2B knockdown model, we assessed cellular proliferation and expression of hypoxia-inducible factor1α (HIF-1α). We examined the adenosine receptor expression profile under both normoxic and hypoxic conditions in the OSCC-derived cells. In addition to in vitro data, the clinical correlation between the ADORA2B expression levels in primary OSCCs (n = 100 patients) and the clinicopathological status by immunohistochemistry (IHC) also was evaluated.

resultsADORA2B mRNA and protein were up-regulated significantly (p < 0.05) in seven OSCC-derived cells compared with human normal oral keratinocytes. Suppression of ADORA2B expression with shRNA significantly (p < 0.05) inhibited cellular proliferation compared with the control cells. HIF-1α also was down-regulated in ADORA2B knockdown OSCC cells. During hypoxia, ADORA2B expression was induced significantly (p < 0.05) in the mRNA and protein after 24 hours of incubation in OSCC-derived cells. IHC showed that ADORA2B expression in primary OSCCs was significantly (p < 0.05) greater than in the normal oral counterparts and that ADORA2B-positive OSCCs were correlated closely (p < 0.05) with tumoral size.

conclusionOur results suggested that ADORA2B controls cellular proliferation via HIF-1α activation, indicating that ADORA2B may be a key regulator of tumoral progression in OSCCs.

Indexed as

AgedCarcinoma, Squamous CellCell HypoxiaCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiddle AgedMouth NeoplasmsReceptor, Adenosine A2BUp-RegulationHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitReceptor, Adenosine A2B

Identifiers

PMID26228921
PMCPMC4520274
OpenAlexW1493633378

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.