Evidence map›Paper›PMID 28397110›Full record

ArticlePurinergic signalling2017

Potential role of P2X7R in esophageal squamous cell carcinoma proliferation.

André A Santos, Angélica R Cappellari, Fernanda O de Marchi, Marina P Gehring, Aline Zaparte, Caroline A Brandão, Tiago Giuliani Lopes, Vinicius D da Silva, Luis Felipe Ribeiro Pinto, Luiz Eduardo Baggio Savio and 5 more

Abstract read
In one paragraph

Article in Purinergic signalling, 2017. 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
2.0field-weighted citation impact, top 15% 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, 37 citations in OpenAlex.

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  12. P2X7 receptor: a critical regulator and potential target for breast cancer.Journal of molecular medicine (Berlin, Germany) · 2021
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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

15 authors at 6 institutions in 2 countries.

André A SantosPrograma de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Angélica R CappellariPrograma de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Fernanda O de MarchiFaculdade de Farmácia, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Marina P GehringPrograma de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Aline ZapartePrograma de Pós-graduação em Medicina e Ciências da Saúde, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Caroline A BrandãoFaculdade de Medicina, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Tiago Giuliani LopesHospital São Lucas da PUCRS, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Vinicius D da SilvaPrograma de Pós-graduação em Medicina e Ciências da Saúde, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Luis Felipe Ribeiro PintoPrograma de Carcinogênese Molecular, Coordenação de Pesquisa, Instituto Nacional do Câncer (INCA), Rio de Janeiro, Brazil.
Luiz Eduardo Baggio SavioInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Aline Cristina Abreu Moreira-SouzaInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Robson Coutinho-SilvaInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Juliano D PaccezInternational Centre for Genetic Engineering and Biotechnology (ICGEB), Cancer Genomics Group, Cape Town, South Africa.
Luiz F ZerbiniInternational Centre for Genetic Engineering and Biotechnology (ICGEB), Cancer Genomics Group, Cape Town, South Africa.
Fernanda B MorronePrograma de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil. fernanda.morrone@pucrs.br.
Pontifícia Universidade Católica do Rio Grande do Sul · BRUniversidade Federal do Rio de Janeiro · BRHospital São Lucas da PUCRS · BRInstituto Nacional do Câncer · BRInternational Centre for Genetic Engineering and Biotechnology · ZAUniversity of Cape Town · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer is an aggressive tumor and is the sixth leading cause of cancer death worldwide. ATP is well known to regulate cancer progression in a variety of models by different mechanisms, including P2X7R activation. This study aimed to evaluate the role of P2X7R in esophageal squamous cell carcinoma (ESCC) proliferation. Our results show that treatment with high ATP concentrations induced a decrease in cell number, cell viability, number of polyclonal colonies, and reduced migration of ESCC. The treatment with the selective P2X7R antagonist A740003 or siRNA for P2X7 reverted this effect in the KYSE450 cell line. In addition, results showed that P2X7R is highly expressed, at mRNA and protein levels, in KYSE450 lineage. Additionally, KYSE450, KYSE30, and OE21 cells express P2X3R, P2X4R, P2X5R, P2X6R, and P2X7R genes. P2X1R is expressed by KYSE30 and KYSE450, and only KYSE450 expresses the P2X2R gene. Furthermore, esophageal cancer cell line KYSE450 presented higher expression of E-NTPDases 1 and 2 and of Ecto-5'-NT/CD73 when compared to normal cells. This cell line also exhibits ATPase, ADPase, and AMPase activity, although in different levels, and the co-treatment of apyrase was able to revert the antiproliferative effects of ATP. Moreover, results showed high immunostaining for P2X7R in biopsies of patients with esophageal carcinoma, indicating the involvement of this receptor in the growth of this type of cancer. The results suggest that P2X7R may be a potential pharmacological target to treat ESCC and can lead us to further investigate the effect of this receptor in cancer cell progression.

Indexed as

Adenosine TriphosphateCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell SurvivalEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansReceptors, Purinergic P2X7RNA, Small InterferingAdenosine TriphosphateP2RX7 protein, humanReceptors, Purinergic P2X7RNA, Small InterferingATPEctonucleotidasesEsophageal cancerP2X7RProliferation

Identifiers

PMID28397110
PMCPMC5563289
OpenAlexW2607121638

What OpenQuestion holds

Textmetadata
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.