Evidence map›Paper›PMID 28422142›Full record

ArticleScientific reports2017

G protein-coupled KISS1 receptor is overexpressed in triple negative breast cancer and promotes drug resistance.

Alexandra Blake, Magdalena Dragan, Rommel G Tirona, Daniel B Hardy, Muriel Brackstone, Alan B Tuck, Andy V Babwah, Moshmi Bhattacharya

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

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.8field-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

33 citing papers in PubMed, 46 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

8 authors at 3 institutions in 2 countries.

Alexandra BlakeDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Magdalena DraganDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Rommel G TironaDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Daniel B HardyDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Muriel BrackstoneLawson Health Research Institute, London, ON, Canada.
Alan B TuckDepartment of Oncology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Andy V BabwahDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Moshmi BhattacharyaDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON, Canada.
Western University · CALawson Health Research Institute · CALondon Cancer · GB

Funding

CIHR MOP 107972CIHR PJT-148823
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) lacks the expression of estrogen receptor α, progesterone receptor and human epidermal growth factor receptor 2 (HER2). TNBC patients lack targeted therapies, as they fail to respond to endocrine and anti-HER2 therapy. Prognosis for this aggressive cancer subtype is poor and survival is limited due to the development of resistance to available chemotherapies and resultant metastases. The mechanisms regulating tumor resistance are poorly understood. Here we demonstrate that the G protein-coupled kisspeptin receptor (KISS1R) promotes drug resistance in TNBC cells. KISS1R binds kisspeptins, peptide products of the KISS1 gene and in numerous cancers, this signaling pathway plays anti-metastatic roles. However, in TNBC, KISS1R promotes tumor invasion. We show that KISS1 and KISS1R mRNA and KISS1R protein are upregulated in TNBC tumors, compared to normal breast tissue. KISS1R signaling promotes drug resistance by increasing the expression of efflux drug transporter, breast cancer resistance protein (BCRP) and by inducing the activity and transcription of the receptor tyrosine kinase, AXL. BCRP and AXL transcripts are elevated in TNBC tumors, compared to normal breast, and TNBC tumors expressing KISS1R also express AXL and BCRP. Thus, KISS1R represents a potentially novel therapeutic target to restore drug sensitivity in TNBC patients.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticATP Binding Cassette Transporter, Subfamily G, Member 2Axl Receptor Tyrosine KinaseCell Line, TumorFemaleHumansKisspeptinsNeoplasm InvasivenessNeoplasm ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Kisspeptin-1Triple Negative Breast NeoplasmsABCG2 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 2AXL protein, humanAxl Receptor Tyrosine KinaseKISS1 protein, humanKISS1R protein, humanKisspeptinsNeoplasm ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Kisspeptin-1

Identifiers

PMID28422142
PMCPMC5395950
OpenAlexW2607038075

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.