Evidence map›Paper›PMID 29123257›Full record

ArticleBritish journal of cancer2018

Prostaglandin receptors induce urothelial tumourigenesis as well as bladder cancer progression and cisplatin resistance presumably via modulating PTEN expression.

Eiji Kashiwagi, Satoshi Inoue, Taichi Mizushima, Jinbo Chen, Hiroki Ide, Takashi Kawahara, Leonardo O Reis, Alexander S Baras, George J Netto, Hiroshi Miyamoto

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

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

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  20. Eicosanoids in Cancer: Prostaglandin EFrontiers in pharmacology · 2020
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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

10 authors at 2 institutions in 1 country.

Eiji KashiwagiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Satoshi InoueDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Taichi MizushimaDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Jinbo ChenDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Hiroki IdeDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Takashi KawaharaDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Leonardo O ReisDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Alexander S BarasDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
George J NettoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Hiroshi MiyamotoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins Medicine · USUniversity of Rochester Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe investigated the role of prostaglandin receptors (e.g. prostaglandin E2 receptor 2 (EP2), EP4) and the efficacy of celecoxib in urothelial tumourigenesis and cancer progression.

methodsWe performed immunohistochemistry in bladder cancer (BC) tissue microarrays, in vitro transformation assay in a normal urothelial SVHUC line, and western blot/reverse transcription-polymerase chain reaction/cell growth assays in BC lines.

resultsEP2/EP4 expression was elevated in BCs compared with non-neoplastic urothelial tissues and in BCs from those who were resistant to cisplatin-based neoadjuvant chemotherapy. Strong positivity of EP2/EP4 in non-muscle-invasive tumours or positivity of EP2/EP4 in muscle-invasive tumours strongly correlated with disease progression or disease-specific mortality, respectively. In SVHUC cells, exposure to a chemical carcinogen 3-methylcholanthrene considerably increased and decreased the expression of EP2/EP4 and phosphatase and tensin homologue (PTEN), respectively. Treatment with selective EP2/EP4 antagonist or celecoxib also resulted in prevention in 3-methylcholanthrene-induced neoplastic transformation of SVHUC cells. In BC lines, EP2/EP4 antagonists and celecoxib effectively inhibited cell viability and migration, as well as augmented PTEN expression. Furthermore, these drugs enhanced the cytotoxic activity of cisplatin in BC cells. EP2/EP4 and PTEN were also elevated and reduced, respectively, in cisplatin-resistant BC sublines.

conclusionsEP2/EP4 activation correlates with induction of urothelial cancer initiation and outgrowth, as well as chemoresistance, presumably via downregulating PTEN expression.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell MovementCell ProliferationCisplatinDrug Resistance, NeoplasmHeterograftsHumansImmunohistochemistryMaleMiceMice, Inbred NODMice, SCIDNeoplasm InvasivenessPTEN PhosphohydrolaseAntineoplastic AgentsCisplatinPTEN PhosphohydrolasePTEN protein, humanReceptors, Prostaglandin

Identifiers

PMID29123257
PMCPMC5785746
OpenAlexW2767755063

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.