Evidence map›Paper›PMID 30456574›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2019

CCR5 blockage by maraviroc: a potential therapeutic option for metastatic breast cancer.

Asim Pervaiz, Michael Zepp, Saqib Mahmood, Doaa Mohamed Ali, Martin R Berger, Hassan Adwan

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 68 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

6 authors at 2 institutions in 3 countries.

Asim PervaizInstitute of Biomedical and Allied Health Sciences, University of Health Sciences, Lahore, Pakistan.
Michael ZeppToxicology and Chemotherapy Unit, German Cancer Research Centre (DKFZ), Im Neuenheimer Feld 581, 69120, Heidelberg, Germany.
Saqib MahmoodInstitute of Biomedical and Allied Health Sciences, University of Health Sciences, Lahore, Pakistan.
Doaa Mohamed AliToxicology and Chemotherapy Unit, German Cancer Research Centre (DKFZ), Im Neuenheimer Feld 581, 69120, Heidelberg, Germany.
Martin R BergerToxicology and Chemotherapy Unit, German Cancer Research Centre (DKFZ), Im Neuenheimer Feld 581, 69120, Heidelberg, Germany. m.berger@dkfz.de.ORCID http://orcid.org/0000-0002-3783-5365
Hassan AdwanToxicology and Chemotherapy Unit, German Cancer Research Centre (DKFZ), Im Neuenheimer Feld 581, 69120, Heidelberg, Germany.
German Cancer Research Center · DEUniversity of Health Sciences Lahore · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeBone metastasis is observed in up to 70% of breast cancer patients. The currently available treatment options are palliative in nature. Chemokine receptor 5 (CCR5) has gained attention as therapeutic target in various malignancies. Here, we investigated the effects of targeting CCR5 by its antagonist maraviroc in metastatic breast cancer cells.

methodsIn response to maraviroc exposure, cytotoxicity was assessed using an MTT proliferation assay, whereas the effects on colony formation and migration were assessed using colony formation, transwell chamber migration and scratch wound healing assays, respectively. Apoptosis-related activities were investigated using nuclear staining, annexin-V FITC staining and Western blotting. Cell cycle changes were analysed using flow cytometry and qRT-PCR for cell cycle relevant genes. A nude rat model for breast cancer bone metastasis was used to evaluate the in vivo efficacy of CCR5 targeting by maraviroc. Circulatory levels of the three cognate ligands for CCR5 (CCL3, CCL4, CCL5) were analysed in sera of breast cancer patients using ELISA.

resultsWe found that blockade of CCR5 attenuated the proliferation, colony formation and migration of metastatic breast cancer cells, and induced apoptosis and arrest in the G1 phase of the cell cycle. Expression profiling highlighted the involvement of cell cycle related signalling cascades. We also found that treatment with maraviroc significantly inhibited bone metastasis in nude rats implanted with MDA-MB-231 breast cancer cells. Finally, we found that the circulatory levels of three cognate ligands for the CCR5 receptor varied between breast cancer patients and healthy controls.

conclusionOur findings indicate that targeting CCR5 may be an effective strategy to combat breast cancer bone metastasis.

Indexed as

AdultAnimalsApoptosisBone NeoplasmsBreast NeoplasmsCase-Control StudiesCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleG1 PhaseHumansLigandsMaravirocCCR5 protein, humanLigandsMaravirocReceptors, CCR5ApoptosisBone metastasisBreast cancerCCR5Cell cycle arrestMaraviroc

Identifiers

PMID30456574
PMCPMC12994360
OpenAlexW2901325045

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.