Evidence map›Paper›PMID 34038868›Full record

ArticleAging2021

Inhibition of CXCR2 plays a pivotal role in re-sensitizing ovarian cancer to cisplatin treatment.

Taciane Barbosa Henriques, Diandra Zipinotti Dos Santos, Isabella Dos Santos Guimarães, Nayara Gusmão Tessarollo, Paulo Cilas Morais Lyra-Junior, Patricia Mesquita, Diana Pádua, Ana Luisa Amaral, Bruno Cavadas, Luisa Pereira and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 37 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Taciane Barbosa HenriquesBiotechnology Program/RENORBIO, Health Sciences Center, Federal University of Espirito Santo, Espirito Santo, Brazil.
Diandra Zipinotti Dos SantosBiotechnology Program/RENORBIO, Health Sciences Center, Federal University of Espirito Santo, Espirito Santo, Brazil.
Isabella Dos Santos GuimarãesTranslational Research Laboratory/Division of Clinical Research and Technological Development/National Cancer Institute (INCa), Rio de Janeiro, Brazil.
Nayara Gusmão TessarolloBiotechnology Program/RENORBIO, Health Sciences Center, Federal University of Espirito Santo, Espirito Santo, Brazil.
Paulo Cilas Morais Lyra-JuniorBiotechnology Program/RENORBIO, Health Sciences Center, Federal University of Espirito Santo, Espirito Santo, Brazil.
Patricia MesquitaInstituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto, Portugal.
Diana PáduaInstituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto, Portugal.
Ana Luisa AmaralInstituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto, Portugal.
Bruno CavadasInstituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto, Portugal.
Luisa PereiraInstituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto, Portugal.
Ian Victor SilvaDepartment of Morphology, Health Sciences Center, Federal University of Espirito Santo, Espirito Santo, Brazil.
Raquel Maria da Silva Graça AlmeidaInstituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto, Portugal.
Leticia Batista Azevedo RangelBiotechnology Program/RENORBIO, Health Sciences Center, Federal University of Espirito Santo, Espirito Santo, Brazil.
Universidade do Porto · PTUniversidade Federal do Espírito Santo · BRInstituto Nacional do Câncer · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

cDNA microarray data conducted by our group revealed overexpression of CXCL2 and CXCL8 in ovarian cancer (OC) microenvironment. Herein, we have proven that the chemokine receptor, CXCR2, is a pivotal molecule in re-sensitizing OC to cisplatin, and its inhibition decreases cell proliferation, viability, tumor size in cisplatin-resistant cells, as well as reversed the overexpression of mesenchymal epithelium transition markers. Altogether, our study indicates a central effect of CXCR2 in preventing tumor progression, due to acquisition of cisplatin chemoresistant phenotype by tumor cells, and patients' high lethality rate. We found that the overexpression of CXCR2 by OC cells is persistent and anomalously confined to the cellular nuclei, thus pointing to an urge in developing highly lipophilic molecules that promptly permeate cells, bind to and inhibit nuclear CXCR2 to fight OC, instead of relying on the high-cost genetic engineered cells.

Indexed as

AnimalsCell Line, TumorCell NucleusCell ProliferationCell SurvivalChemokine CXCL2Chick EmbryoCisplatinDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleHumansMAP Kinase Signaling SystemNeoplasm InvasivenessNeoplasm ProteinsNeovascularization, PathologicChemokine CXCL2CisplatinNeoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Interleukin-8BTOR Serine-Threonine KinaseschemoresistanceCXCR2high grade serous ovarian cancertumor microenvironment

Identifiers

PMID34038868
PMCPMC8202899
OpenAlexW3164285033

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.