Evidence map›Paper›PMID 24738946›Full record

ArticleACS chemical biology2014

Inositol phosphate recycling regulates glycolytic and lipid metabolism that drives cancer aggressiveness.

Daniel I Benjamin, Sharon M Louie, Melinda M Mulvihill, Rebecca A Kohnz, Daniel S Li, Lauryn G Chan, Antonio Sorrentino, Sourav Bandyopadhyay, Alyssa Cozzo, Anayo Ohiri and 3 more

Open access · greenAbstract read
In one paragraph

Article in ACS chemical biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 51 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

13 authors at 2 institutions in 1 country.

Daniel I BenjaminProgram in Metabolic Biology, Department of Nutritional Sciences and Toxicology, University of California, Berkeley , Berkeley, California 94720, United States.
Sharon M Louie
Melinda M Mulvihill
Rebecca A Kohnz
Daniel S Li
Lauryn G Chan
Antonio Sorrentino
Sourav Bandyopadhyay
Alyssa Cozzo
Anayo Ohiri
Andrei Goga
Shu-Wing Ng
Daniel K Nomura
University of California, Berkeley · USBrigham and Women's Hospital · US

Funding

UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Holger Willenbring · 1986 to 2026
$30.7M
Pre-doctoral Training in Molecular and Biochemical NutritionT32DK061918 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2002 to 2016
$2.6M
In Vivo Metabolic Catastrophe Is Induced By Acute Oncogene Inhibition (PQ #22)R01CA170447 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2012 to 2015
$2.4M
Targeting the MYC Oncogene with CDK InhibitorsR01CA136717 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2010 to 2014
$1.8M
Annotating the Role of Dysregulated Inositol Phosphate Metabolism in Malignant CaR01CA172667 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI NOMURA, DANIEL · 2013 to 2017
$1.7M
Role of monoacylglycerol lipase in coordinating diverse lipid signaling pathwaysR00DA030908 · NIDA · UNIVERSITY OF CALIFORNIA BERKELEY · PI NOMURA, DANIEL · 2011 to 2013
$723k
Targeting lipid metabolic and signaling enzyme in ovarian cancerR21CA150237 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI NG, SHU-WING · 2010 to 2011
$449k
Remodeling of Dietary Fat into Protumorigenic Signaling Lipids in Cancer (PQ1)R21CA170317 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI NOMURA, DANIEL · 2012 to 2013
$342k
NCI NIH HHS 1R21CA150237NCI NIH HHS 5R01CA136717NCI NIH HHS 5R01CA17044 7NCI NIH HHS R01 CA136717NCI NIH HHS R01 CA170447NCI NIH HHS R01 CA172667NCI NIH HHS R01CA172667NCI NIH HHS R21 CA150237NCI NIH HHS R21 CA170317NCI NIH HHS R21CA170317NIDA NIH HHS R00 DA030908NIDA NIH HHS R00DA030908NIDDK NIH HHS P30 DK026743NIDDK NIH HHS T32 DK061918
6 · The paper itself

Abstract

Cancer cells possess fundamentally altered metabolism that supports their pathogenic features, which includes a heightened reliance on aerobic glycolysis to provide precursors for synthesis of biomass. We show here that inositol polyphosphate phosphatase 1 (INPP1) is highly expressed in aggressive human cancer cells and primary high-grade human tumors. Inactivation of INPP1 leads to a reduction in glycolytic intermediates that feed into the synthesis of the oncogenic signaling lipid lysophosphatidic acid (LPA), which in turn impairs LPA signaling and further attenuates glycolytic metabolism in a feed-forward mechanism to impair cancer cell motility, invasiveness, and tumorigenicity. Taken together these findings reveal a novel mode of glycolytic control in cancer cells that can serve to promote key oncogenic lipid signaling pathways that drive cancer pathogenicity.

Indexed as

AnimalsApoptosisBlotting, WesternCarcinoma, PapillaryCell MovementCell ProliferationCystadenocarcinoma, SerousFemaleGlycolysisHumansInositol PhosphatesLipid MetabolismMetabolomeMiceMice, SCIDNeoplasmsinositol-1,4-bisphosphate 1-phosphataseInositol PhosphatesPhosphoric Monoester HydrolasesRNA, Small Interfering

Identifiers

PMID24738946
PMCPMC4076040
OpenAlexW2142554748

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.