Evidence map›Paper›PMID 29395055›Full record

ArticleCell stem cell2018

Phospholipid Remodeling and Cholesterol Availability Regulate Intestinal Stemness and Tumorigenesis.

Bo Wang, Xin Rong, Elisa N D Palladino, Jiafang Wang, Alan M Fogelman, Martín G Martín, Waddah A Alrefai, David A Ford, Peter Tontonoz

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

Article in Cell stem cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 2 pooled it
12.1field-weighted citation impact, top 1% 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

189 citing papers in PubMed, 2 syntheses or guidelines pooled it, 314 citations in OpenAlex.

  1. Pooled it
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  9. The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026
    Review
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129 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Bo WangDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Xin RongDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Elisa N D PalladinoDepartment of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University, St. Louis, MO, USA.
Jiafang WangDepartment of Pediatrics, Division of Gastroenterology and Nutrition, Mattel Children's Hospital, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Alan M FogelmanDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Martín G MartínDepartment of Pediatrics, Division of Gastroenterology and Nutrition, Mattel Children's Hospital, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Waddah A AlrefaiResearch and Development, Jesse Brown VA Medical Center, Chicago, IL, USA; Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
David A FordDepartment of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University, St. Louis, MO, USA.
Peter TontonozDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA. Electronic address: ptontonoz@mednet.ucla.edu.
University of California, Los Angeles · USSaint Louis University · USMattel Children's Hospital · USUniversity of Illinois Chicago · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 1985 to 2019
$55.2M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Andrea L Hevener · 2003 to 2026
$40.4M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Intestinal Stem Cell Consortium Coordinating CenterU01DK085532 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NILAND, JOYCE CAROL · 2009 to 2018
$6.5M
Intestinal Stem Cell Culture and Entero-Endocrine Lineage DevelopmentU01DK085535 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUNN, JAMES C, MARTIN, MARTIN G · 2009 to 2018
$3.7M
Limited Competition for the Continuation of the Intestinal Stem Cell Consortium Coordinating CenterU24DK085532 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NILAND, JOYCE CAROL · 2019 to 2023
$2.3M
The Role of Lpcat3 and Phospholipid Remodeling in Intestinal HomeostasisK01DK114373 · NIDDK · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI WANG, BO · 2018 to 2022
$769k
NHLBI NIH HHS P01 HL030568NIDDK NIH HHS K01 DK114373NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P30 DK063491NIDDK NIH HHS U01 DK085532NIDDK NIH HHS U01 DK085535NIDDK NIH HHS U24 DK085532
6 · The paper itself

Abstract

Adequate availability of cellular building blocks, including lipids, is a prerequisite for cellular proliferation, but excess dietary lipids are linked to increased cancer risk. Despite these connections, specific regulatory relationships between membrane composition, intestinal stem cell (ISC) proliferation, and tumorigenesis are unclear. We reveal an unexpected link between membrane phospholipid remodeling and cholesterol biosynthesis and demonstrate that cholesterol itself acts as a mitogen for ISCs. Inhibition of the phospholipid-remodeling enzyme Lpcat3 increases membrane saturation and stimulates cholesterol biosynthesis, thereby driving ISC proliferation. Pharmacologic inhibition of cholesterol synthesis normalizes crypt hyperproliferation in Lpcat3-deficient organoids and mice. Conversely, increasing cellular cholesterol content stimulates crypt organoid growth, and providing excess dietary cholesterol or driving endogenous cholesterol synthesis through SREBP-2 expression promotes ISC proliferation in vivo. Finally, disruption of Lpcat3-dependent phospholipid and cholesterol homeostasis dramatically enhances tumor formation in Apc

Indexed as

1-Acylglycerophosphocholine O-AcyltransferaseAnimalsBiosynthetic PathwaysCarcinogenesisCell ProliferationCholesterolIntestinesMiceOrganoidsPhospholipidsStem Cells1-Acylglycerophosphocholine O-AcyltransferaseCholesterolLPCAT3 protein, mousePhospholipidscholesterolintestinal stem cellphospholipid

Identifiers

PMID29395055
PMCPMC5807072
OpenAlexW2784611114

What OpenQuestion holds

Textmetadata
LicenceTDM
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.