Evidence map›Paper›PMID 25204426›Full record

ArticleScientific reports2014

Stage of breast cancer progression influences cellular response to activation of the WNT/planar cell polarity pathway.

Connor D MacMillan, Hon S Leong, David W Dales, Amy E Robertson, John D Lewis, Ann F Chambers, Alan B Tuck

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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, 45 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Connor D MacMillan1] Department of Pathology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON [2] London Regional Cancer Program, London Health Sciences Centre, London, ON [3] Department of Surgery, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON.
Hon S Leong1] London Regional Cancer Program, London Health Sciences Centre, London, ON [2] Department of Surgery, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON.
David W DalesLondon Regional Cancer Program, London Health Sciences Centre, London, ON.
Amy E Robertson1] London Regional Cancer Program, London Health Sciences Centre, London, ON [2] Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON.
John D LewisDepartment of Oncology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB.
Ann F Chambers1] Department of Pathology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON [2] London Regional Cancer Program, London Health Sciences Centre, London, ON [3] Department of Oncology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON [4] Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON.
Alan B Tuck1] Department of Pathology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON [2] London Regional Cancer Program, London Health Sciences Centre, London, ON [3] Department of Oncology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON.
London Health Sciences Centre · CAUniversity of Alberta · CAWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Planar cell polarity (PCP) signaling has been shown in different studies to either promote or inhibit the malignancy of breast cancer. Using the 21T cell lines, which were derived from an individual patient and represent distinct stages of progression, we show that the prototypical PCP ligand, WNT5A, is expressed highest in 21MT-1 cells (invasive mammary carcinoma) and lowest in 21PT (atypical ductal hyperplasia) and 21NT (ductal carcinoma in situ) cells. Overexpression of WNT5A decreased spherical colony formation and increased invasion and in vivo extravasation only in 21NT cells; whereas overexpression increased migration of both 21PT and 21NT cells. WNT5A overexpression also increased RHOA expression of both cell lines and subsequent RHOA knockdown blocked WNT5A-induced migration, but only partially blocked WNT5A-induced invasion of 21NT cells. PCP can signal through VANGL1 to modulate AP-1 target genes (e.g. MMP3) and induce invasion. VANGL1 knockdown inhibited WNT5A-induced invasion of 21NT cells, but had no effect on WNT5A-induced migration of either 21PT or 21NT cells. WNT5A-induced MMP3 expression was seen only in 21NT cells, an effect that was VANGL1 dependent, but independent of AP-1. We thus provide evidence that PCP signaling can act in a context dependent manner to promote breast cancer progression.

Indexed as

Breast NeoplasmsCarrier ProteinsCell Line, TumorCell MovementCell PolarityCyclooxygenase 2Disease ProgressionFemaleHumansMatrix Metalloproteinase 3Membrane ProteinsNeoplasm InvasivenessProto-Oncogene ProteinsrhoA GTP-Binding ProteinRNA InterferenceRNA, MessengerCarrier ProteinsCyclooxygenase 2Matrix Metalloproteinase 3Membrane ProteinsMMP3 protein, humanProto-Oncogene ProteinsPTGS2 protein, humanrhoA GTP-Binding ProteinRHOA protein, humanRNA, MessengerRNA, Small InterferingTranscription Factor AP-1VANGL1 protein, humanWnt-5a ProteinWNT5A protein, humanWnt Proteins

Identifiers

PMID25204426
PMCPMC4159636
OpenAlexW2015495442

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.