Evidence map›Paper›PMID 24606897›Full record

ArticleCell metabolism2014

Cholesteryl ester accumulation induced by PTEN loss and PI3K/AKT activation underlies human prostate cancer aggressiveness.

Shuhua Yue, Junjie Li, Seung-Young Lee, Hyeon Jeong Lee, Tian Shao, Bing Song, Liang Cheng, Timothy A Masterson, Xiaoqi Liu, Timothy L Ratliff and 1 more

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

Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 528 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
528citing papers in PubMed, 3 pooled it
16.0field-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

528 citing papers in PubMed, 3 syntheses or guidelines pooled it, 927 citations in OpenAlex.

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468 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Shuhua YueWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA.
Junjie LiDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Seung-Young LeeWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA.
Hyeon Jeong LeeDepartment of Comparative Pathobiology, Purdue University, West Lafayette, IN 47907, USA.
Tian ShaoDepartment of Biochemistry, Purdue University, West Lafayette, IN 47907, USA.
Bing SongDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Liang ChengDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Timothy A MastersonDepartment of Urology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Xiaoqi LiuDepartment of Biochemistry, Purdue University, West Lafayette, IN 47907, USA; Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA.
Timothy L RatliffDepartment of Comparative Pathobiology, Purdue University, West Lafayette, IN 47907, USA; Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA.
Ji-Xin ChengWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA; Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA. Electronic address: jcheng@purdue.edu.
Purdue University West Lafayette · USCenter for Cancer Research · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Plk1 in Chemo-resistance of CancerR01CA157429 · NCI · UNIVERSITY OF KENTUCKY · PI XIAOQI LIU · 2011 to 2026
$3.5M
Quantitative Spectroscopic Imaging of Cancer Metabolites in Live Cells and IntactR21CA182608 · NCI · PURDUE UNIVERSITY · PI CHENG, JI-XIN · 2013 to 2015
$654k
NCI NIH HHS R01 CA157429NCI NIH HHS R21 CA182608
6 · The paper itself

Abstract

Altered lipid metabolism is increasingly recognized as a signature of cancer cells. Enabled by label-free Raman spectromicroscopy, we performed quantitative analysis of lipogenesis at single-cell level in human patient cancerous tissues. Our imaging data revealed an unexpected, aberrant accumulation of esterified cholesterol in lipid droplets of high-grade prostate cancer and metastases. Biochemical study showed that such cholesteryl ester accumulation was a consequence of loss of tumor suppressor PTEN and subsequent activation of PI3K/AKT pathway in prostate cancer cells. Furthermore, we found that such accumulation arose from significantly enhanced uptake of exogenous lipoproteins and required cholesterol esterification. Depletion of cholesteryl ester storage significantly reduced cancer proliferation, impaired cancer invasion capability, and suppressed tumor growth in mouse xenograft models with negligible toxicity. These findings open opportunities for diagnosing and treating prostate cancer by targeting the altered cholesterol metabolism.

Indexed as

Acetyl-CoA C-AcetyltransferaseAnimalsCell Line, TumorCell MovementCell ProliferationCell SurvivalCholesterolCholesterol EstersHumansMaleMiceMice, NudePhosphatidylinositol 3-KinaseProstatic NeoplasmsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseACAT1 protein, humanAcetyl-CoA C-AcetyltransferaseCholesterolCholesterol EstersPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanReceptors, AndrogenReceptors, LDL

Identifiers

PMID24606897
PMCPMC3969850
OpenAlexW2032860037

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.