Evidence map›Paper›PMID 30154249›Full record

ArticleMolecular cancer research : MCR2019

Naser Jafari, James Drury, Andrew J Morris, Fredrick O Onono, Payton D Stevens, Tianyan Gao, Jinpeng Liu, Chi Wang, Eun Y Lee, Heidi L Weiss and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

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  12. Multiple-matrix metabolomics analysis for the distinct detection of colorectal cancer and adenoma.Metabolomics : Official journal of the Metabolomic Society · 2024
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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

12 authors at 2 institutions in 1 country.

Naser JafariDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky.
James DruryDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky.
Andrew J MorrisMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
Fredrick O OnonoMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
Payton D StevensDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky.
Tianyan GaoMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
Jinpeng LiuMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
Chi WangMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
Eun Y LeeDepartment of Pathology and Laboratory Medicine, University of Kentucky, Lexington, Kentucky.
Heidi L WeissMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
B Mark EversMarkey Cancer Center, University of Kentucky, Lexington, Kentucky.
Yekaterina Y ZaytsevaDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky. yyzayt2@uky.edu.
University of Kentucky · USMarkey Cancer Center · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
University of Kentucky Center for Cancer MetabolismP20GM121327 · NIGMS · UNIVERSITY OF KENTUCKY · PI Jianhang Jia · 2017 to 2026
$25.0M
The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI KATZ, WENDY S · 2012 to 2017
$13.7M
Pilot Projects ProgramP30GM127211 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2018 to 2022
$5.7M
The Role of PHLPP in Colon CancerR01CA133429 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GAO, TIANYAN · 2009 to 2024
$5.6M
TRAINING GRANT IN MOLECULAR MECHANISMS OF TOXICITY.T32ES007266 · NIEHS · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI, MELLON, ISABEL W · 1990 to 2020
$3.7M
Altered Lipid Metabolism as a Novel Target for Colon Cancer TreatmentR01CA208343 · NCI · UNIVERSITY OF KENTUCKY · PI EVERS, BERNARD MARK, GAO, TIANYAN · 2017 to 2021
$2.1M
Targeting Lipid Metabolism in Colorectal CancerR01CA249734 · NCI · UNIVERSITY OF KENTUCKY · PI ZAYTSEVA, YEKATERINA · 2021 to 2025
$1.7M
Triple Quadrupole Mass Spectrometer SystemS10OD021753 · OD · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2017 to 2017
$352k
The Role of Fatty Acid Synthase in Regulation of Cancer Cells Survival and Metastasis in Colorectal CancerK22CA197193 · NCI · UNIVERSITY OF KENTUCKY · PI ZAYTSEVA, YEKATERINA · 2016 to 2016
$158k
Lysophosphatidic acid and cardiovascular disease riskI01CX001550 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI MORRIS, ANDREW J · 2017 to 2021
–
CSRD VA I01 CX001550NCI NIH HHS K22 CA197193NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA133429NCI NIH HHS R01 CA208343NCI NIH HHS R01 CA249734NIEHS NIH HHS T32 ES007266NIGMS NIH HHS P20 GM103527NIGMS NIH HHS P20 GM121327NIGMS NIH HHS P30 GM127211NIH HHS S10 OD021753
6 · The paper itself

Abstract

Metastasis is the most common cause of death in colorectal cancer patients. Fatty acid synthase (FASN) and sphingosine kinase-1 and -2 (SPHK1 and 2) are overexpressed in many cancers, including colorectal cancer. However, the contribution of FASN-mediated upregulation of sphingolipid metabolism to colorectal cancer metastasis and the potential of these pathways as targets for therapeutic intervention remain unknown. This study determined that sphingosine kinases (SPHK) are overexpressed in colorectal cancer as compared with normal mucosa. FASN expression significantly correlated with SPHK2 expression in data sets from The Cancer Genome Atlas (TCGA) and a colorectal cancer tumor microarray. FASN, SPHK1, and SPHK2 colocalized within invadopodia of primary colorectal cancer cells. Moreover, FASN inhibition decreased SPHK2 expression and the levels of dihydrosphingosine 1-phosphate (DH-S1P) and sphingosine 1-phosphate (S1P) in colorectal cancer cells and tumor tissues. Inhibition of FASN using TVB-3664 and sphingolipid metabolism using FTY-720 significantly inhibited the ability of primary colorectal cancer cells to proliferate, migrate, form focal adhesions, and degrade gelatin. Inhibition of the FASN/SPHK/S1P axis was accompanied by decreased activation of p-MET, p-FAK, and p-PAX. S1P treatment rescued FASN-mediated inhibition of these proteins, suggesting that FASN promotes metastatic properties of colorectal cancer cells, in part, through an increased sphingolipid metabolism. These data demonstrate that upregulation of the FASN/SPHK/S1P axis promotes colorectal cancer progression by enhancing proliferation, adhesion, and migration. IMPLICATIONS: This study provides a strong rationale for further investigation of the interconnection of

Indexed as

AnimalsCell Line, TumorColorectal NeoplasmsFatty AcidsHumansMiceNeoplasm MetastasisSphingolipidsFatty AcidsSphingolipids

Identifiers

PMID30154249
PMCPMC6318071
OpenAlexW2889378732

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.