Evidence map›Paper›PMID 26366834›Full record

ArticleCell adhesion & migration2015

The cross-talk of LDL-cholesterol with cell motility: insights from the Niemann Pick Type C1 mutation and altered integrin trafficking.

Monira Hoque, Carles Rentero, James R Conway, Rachael Z Murray, Paul Timpson, Carlos Enrich, Thomas Grewal

Open access · goldAbstract read
In one paragraph

Article in Cell adhesion & migration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
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, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

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  11. Cholesterol, Oxysterols and LXRs in Breast Cancer Pathophysiology.International journal of molecular sciences · 2020
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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

7 authors at 5 institutions in 4 countries.

Monira Hoquea Faculty of Pharmacy; University of Sydney ; Sydney , Australia.
Carles Renterob Departament de Biologia Cellular ; Immunologia i Neurociències; Centre de Recerca Biomèdica CELLEX; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Facultat de Medicina; Universitat de Barcelona ; Barcelona , Spain.
James R Conwayc Cancer Research Program; The Kinghorn Cancer Center; Garvan Institute of Medical Research ; Darlinghurst , Australia.
Rachael Z Murrayd Tissue Repair and Regeneration Program; Institute of Health and Biomedical Innovation; Queensland University of Technology ; Brisbane , Australia.
Paul Timpsonc Cancer Research Program; The Kinghorn Cancer Center; Garvan Institute of Medical Research ; Darlinghurst , Australia.
Carlos Enrichb Departament de Biologia Cellular ; Immunologia i Neurociències; Centre de Recerca Biomèdica CELLEX; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Facultat de Medicina; Universitat de Barcelona ; Barcelona , Spain.
Thomas Grewala Faculty of Pharmacy; University of Sydney ; Sydney , Australia.
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESUniversity of Sydney · AUGarvan Institute of Medical Research · AUNational Institute of Biomedical Innovation, Health and Nutrition · JPThe Kinghorn Cancer Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholesterol is considered indispensible for the recruitment and functioning of integrins in focal adhesions for cell migration. However, the physiological cholesterol pools that control integrin trafficking and focal adhesion assembly remain unclear. Using Niemann Pick Type C1 (NPC) mutant cells, which accumulate Low Density lipoprotein (LDL)-derived cholesterol in late endosomes (LE), several recent studies indicate that LDL-cholesterol has multiple roles in regulating focal adhesion dynamics. Firstly, targeting of endocytosed LDL-cholesterol from LE to focal adhesions controls their formation at the leading edge of migrating cells. Other newly emerging literature suggests that this may be coupled to vesicular transport of integrins, Src kinase and metalloproteases from the LE compartment to focal adhesions. Secondly, our recent work identified LDL-cholesterol as a key factor that determines the distribution and ability of several Soluble NSF Attachment Protein (SNAP) Receptor (SNARE) proteins, key players in vesicle transport, to control integrin trafficking to the cell surface and extracellular matrix (ECM) secretion. Collectively, dietary, genetic and pathological changes in cholesterol metabolism may link with efficiency and speed of integrin and ECM cell surface delivery in metastatic cancer cells. This commentary will summarize how direct and indirect pathways enable LDL-cholesterol to modulate cell motility.

Indexed as

Cell MovementAnimalsCholesterol, LDLExtracellular MatrixFocal AdhesionsHumansIntegrinsNeoplasm MetastasisNiemann-Pick Disease, Type CReceptor Cross-TalkSoluble N-Ethylmaleimide-Sensitive Factor Attachment ProteinsCholesterol, LDLIntegrinsSoluble N-Ethylmaleimide-Sensitive Factor Attachment Proteinscell migrationcholesterolintegrin traffickinglate endosomeslow density lipoproteinniemann pick type CSNARE proteinstrans-Golgi-network

Identifiers

PMID26366834
PMCPMC4955373
OpenAlexW1864167487

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.