Evidence map›Paper›PMID 29335545›Full record

ArticleNature genetics2018

An aberrant SREBP-dependent lipogenic program promotes metastatic prostate cancer.

Ming Chen, Jiangwen Zhang, Katia Sampieri, John G Clohessy, Lourdes Mendez, Enrique Gonzalez-Billalabeitia, Xue-Song Liu, Yu-Ru Lee, Jacqueline Fung, Jesse M Katon and 13 more

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

Article in Nature genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 187 papers.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed
11.8field-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

187 citing papers in PubMed, 296 citations in OpenAlex.

  1. Review
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  14. Lipids: Driving Forces in the Underlying Biology of Carcinogenesis.ACS pharmacology & translational science · 2025
    Review
  15. Review
  16. Article
  17. Article
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127 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 8 institutions in 4 countries.

Ming ChenCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jiangwen ZhangSchool of Biological Sciences, University of Hong Kong, Hong Kong, China.
Katia SampieriCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
John G ClohessyCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Lourdes MendezCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Enrique Gonzalez-BillalabeitiaCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Xue-Song LiuCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Yu-Ru LeeCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jacqueline FungCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jesse M KatonCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Archita Venugopal MenonCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Kaitlyn A WebsterCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Christopher NgCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Maria Dilia PalumbieriCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Moussa S DiolombiCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Susanne B BreitkopfDivision of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, MA, USA.
Julie Teruya-FeldsteinDepartment of Pathology, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Sabina SignorettiDepartment of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Roderick T BronsonDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA.
John M AsaraDivision of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, MA, USA.
Mireia Castillo-MartinDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Carlos Cordon-CardoDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.ORCID http://orcid.org/0000-0003-0858-5624
Pier Paolo PandolfiCancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. ppandolf@bidmc.harvard.edu.ORCID http://orcid.org/0000-0002-5352-5295
Beth Israel Deaconess Medical Center · USBrigham and Women's Hospital · USChampalimaud Foundation · PTHarvard University · USIcahn School of Medicine at Mount Sinai · USMemorial Sloan Kettering Cancer Center · USUniversity of Hong Kong · HKUniversity of Siena · IT

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Decoding and Targeting the PI3K-mTOR Signaling Network in CancerR35CA197459 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI BRENDAN D. MANNING · 2015 to 2026
$10.8M
Targeting Tumor Suppressive Pathways for Cancer TherapyR35CA197529 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PANDOLFI, PIER PAOLO · 2015 to 2019
$4.6M
Targeting PML for Leukemia TherapyR01CA142874 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVIGAN, DAVID E. · 2010 to 2020
$4.5M
A metabolic role for PML in tumor suppressionR01CA142780 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PANDOLFI, PIER PAOLO · 2010 to 2014
$1.7M
NCI NIH HHS P01 CA120964NCI NIH HHS R01 CA142780NCI NIH HHS R01 CA142874NCI NIH HHS R35 CA197459NCI NIH HHS R35 CA197529NIH HHS P01CA120964NIH HHS R01CA142780NIH HHS R01CA142874NIH HHS R35CA197459NIH HHS R35CA197529
6 · The paper itself

Abstract

Lipids, either endogenously synthesized or exogenous, have been linked to human cancer. Here we found that PML is frequently co-deleted with PTEN in metastatic human prostate cancer (CaP). We demonstrated that conditional inactivation of Pml in the mouse prostate morphs indolent Pten-null tumors into lethal metastatic disease. We identified MAPK reactivation, subsequent hyperactivation of an aberrant SREBP prometastatic lipogenic program, and a distinctive lipidomic profile as key characteristic features of metastatic Pml and Pten double-null CaP. Furthermore, targeting SREBP in vivo by fatostatin blocked both tumor growth and distant metastasis. Importantly, a high-fat diet (HFD) induced lipid accumulation in prostate tumors and was sufficient to drive metastasis in a nonmetastatic Pten-null mouse model of CaP, and an SREBP signature was highly enriched in metastatic human CaP. Thus, our findings uncover a prometastatic lipogenic program and lend direct genetic and experimental support to the notion that a Western HFD can promote metastasis.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticHumansLipogenesisMaleMetabolic Networks and PathwaysMiceMice, Inbred C57BLMice, KnockoutNeoplasm MetastasisPC-3 CellsProstatic NeoplasmsPTEN PhosphohydrolaseSterol Regulatory Element Binding ProteinsPTEN PhosphohydrolasePten protein, mouseSterol Regulatory Element Binding Proteins

Identifiers

PMID29335545
PMCPMC6714980
OpenAlexW2783366082

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.