Evidence map›Paper›PMID 29634950›Full record

ArticleCancer cell2018

Adipocyte p62/SQSTM1 Suppresses Tumorigenesis through Opposite Regulations of Metabolism in Adipose Tissue and Tumor.

Jianfeng Huang, Angeles Duran, Miguel Reina-Campos, Tania Valencia, Elias A Castilla, Timo D Müller, Matthias H Tschöp, Jorge Moscat, Maria T Diaz-Meco

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Article
  9. Article
  10. The Role of Stroma in Cancer Metabolism.Cold Spring Harbor perspectives in medicine · 2024
    Review
  11. Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

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

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

9 authors at 4 institutions in 2 countries.

Jianfeng HuangCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Angeles DuranCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Miguel Reina-CamposCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA; Sanford Burnham Prebys Graduate School of Biomedical Sciences, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Tania ValenciaCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Elias A CastillaCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Timo D MüllerInstitute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), 85764 Neuherberg, Germany; Division of Metabolic Diseases, Department of Medicine, Technische Universität München, 80333 Munich, Germany.
Matthias H TschöpInstitute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), 85764 Neuherberg, Germany; Division of Metabolic Diseases, Department of Medicine, Technische Universität München, 80333 Munich, Germany.
Jorge MoscatCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: jmoscat@sbpdiscovery.org.
Maria T Diaz-MecoCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: mdmeco@sbpdiscovery.org.
Sanford Burnham Prebys Medical Discovery Institute · USDiscovery Institute · USHelmholtz Zentrum München · DETechnical University of Munich · DE

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Michael Jackson · 1985 to 2026
$107.2M
Role of p62/SQSTM1 in obesity-induced liver cancerR01CA211794 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL, MOSCAT, JORGE · 2017 to 2021
$3.6M
Role of p62 in metabolic reprograming of the tumor stroma in prostate cancerR01CA218254 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DIAZ MECO CONDE, MARIA TERESA, METALLO, CHRISTIAN MICHAEL · 2017 to 2021
$2.6M
The p62/MEKK3 complex in mTORC1 activationR01CA192642 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI DIAZ MECO CONDE, MARIA TERESA · 2015 to 2019
$2.2M
Control of stellate cells-driven liver cancer by the p62/NBR1 adaptersR01DK108743 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MOSCAT, JORGE · 2016 to 2020
$2.2M
NCI NIH HHS P30 CA030199NCI NIH HHS R01 CA192642NCI NIH HHS R01 CA211794NCI NIH HHS R01 CA218254NIDDK NIH HHS R01 DK108743
6 · The paper itself

Abstract

Obesity is a leading risk factor for cancer. However, understanding the crosstalk between adipocytes and tumor cells in vivo, independently of dietary contributions, is a major gap in the field. Here we used a prostate cancer (PCa) mouse model in which the signaling adaptor p62/Sqstm1 is selectively inactivated in adipocytes. p62 loss in adipocytes results in increased osteopontin secretion, which mediates tumor fatty acid oxidation and invasion, leading to aggressive metastatic PCa in vivo. Furthermore, p62 deficiency triggers in adipocytes a general shutdown of energy-utilizing pathways through mTORC1 inhibition, which supports nutrient availability for cancer cells. This reveals a central role of adipocyte's p62 in the symbiotic adipose tissue-tumor collaboration that enables cancer metabolic fitness.

Indexed as

Adipose TissueAnimalsCarnitine O-PalmitoyltransferaseCell Line, TumorCell Transformation, NeoplasticEnergy MetabolismFatty AcidsHumansMaleMiceNeoplasm TransplantationObesityOsteopontinPrognosisProstatic NeoplasmsSequestosome-1 ProteinCarnitine O-PalmitoyltransferaseCPT1A protein, humanFatty AcidsOsteopontinSequestosome-1 ProteinSPP1 protein, humanSQSTM1 protein, humanadipocytecancerCPT1fatty acid oxidationmetabolic reprogrammingobesityosteopontinp62prostatesequestosome-1

Identifiers

PMID29634950
PMCPMC5896786
OpenAlexW2797034406

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.