Evidence map›Paper›PMID 34504181›Full record

ArticleScientific reports2021

Regulation of low-density lipoprotein receptor expression in triple negative breast cancer by EGFR-MAPK signaling.

Tiffany Scully, Nathan Kase, Emily J Gallagher, Derek LeRoith

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Effect ofCancer science · 2023
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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

4 authors at 1 institution in 1 country.

Tiffany ScullyDivision of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1055, New York, NY, 10029, USA.
Nathan KaseDivision of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1055, New York, NY, 10029, USA.
Emily J GallagherDivision of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1055, New York, NY, 10029, USA. Emily.Gallagher@mssm.edu.
Derek LeRoithDivision of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1055, New York, NY, 10029, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

Obesity and triple negative breast cancer; the role of hypercholesterolemiaR01CA200553 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEROITH, DEREK · 2016 to 2020
$1.9M
Cholesterol promotes breast cancer progression: establishing the mechanismsK08CA190770 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GALLAGHER, EMILY JANE · 2014 to 2018
$843k
NCI NIH HHS R01 CA200553NIH HHS K08CA190770
6 · The paper itself

Abstract

Expression of the low-density lipoprotein receptor (LDLR) has been shown to play a critical role in hypercholesterolemia-associated breast cancer growth and is associated with shorter recurrence-free survival in human breast cancer studies. We sought to identify how circulating LDL cholesterol and tumor LDLR might accelerate oncogenic processes by determining whether increased LDLR expression and cholesterol uptake are associated with the activation of the epidermal growth factor receptor (EGFR) signaling pathway in triple negative breast cancer (TNBC) cell lines. EGF stimulation of MDA-MB-468 (MDA468) cells activated p44/42MAPK (MAPK), increased expression of LDLR, and fluorescent LDL cholesterol uptake. However, stimulation of MDA-MB-231 (MDA231) cells with EGF did not lead to increased expression of LDLR despite inducing phosphorylation of EGFR. Inhibition of MAPK using UO126 in MDA231 cells reduced LDLR expression, and in MDA468 cells, UO126 impaired the LDLR increase in response to EGF. MDA468 cells exposed to the transcription inhibitor, Actinomycin, prior to treatment with EGF showed reduced degradation of LDLR mRNA compared to vehicle-treated cells. Our results suggest that the EGF-associated increase in LDLR protein expression is cell line-specific. The common pathway regulating LDLR expression was MAPK in both TNBC cell lines.

Indexed as

AnimalsButadienesCell Line, TumorEpidermal Growth FactorErbB ReceptorsFemaleGene SilencingHumansMAP Kinase Signaling SystemMiceMitogen-Activated Protein KinasesNitrilesPhosphorylationReceptors, LDLRibosomal Protein S6 Kinases, 90-kDaRNA, MessengerButadienesEGFR protein, humanEGFR protein, mouseEpidermal Growth FactorErbB ReceptorsLDLR protein, humanMitogen-Activated Protein KinasesNitrilesReceptors, LDLribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 90-kDaRNA, MessengerRPS6KA1 protein, humanU 0126

Identifiers

PMID34504181
PMCPMC8429745
OpenAlexW3197589846

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.