Evidence map›Paper›PMID 28092677›Full record

ArticleOncogene2017

WNT/β-catenin signaling regulates mitochondrial activity to alter the oncogenic potential of melanoma in a PTEN-dependent manner.

K Brown, P Yang, D Salvador, R Kulikauskas, H Ruohola-Baker, A M Robitaille, A J Chien, R T Moon, V Sherwood

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 63 citations in OpenAlex.

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  16. Article
  17. WNT Signaling in Melanoma.International journal of molecular sciences · 2020
    Review
  18. Review
  19. Non-Apoptotic Cell Death Signaling Pathways in Melanoma.International journal of molecular sciences · 2020
    Review
  20. Review
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.

K BrownSchool of Pharmacy, University of East Anglia, Norwich Research Park, Norwich, UK.
P YangDepartment of Pharmacology, Howard Hughes Medical Institute, Institute for Stem Cell and Regenerative Medicine, Seattle, WA, USA.
D SalvadorDivision of Cancer Research, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
R KulikauskasDepartment of Pharmacology, Howard Hughes Medical Institute, Institute for Stem Cell and Regenerative Medicine, Seattle, WA, USA.
H Ruohola-BakerDepartment of Biochemistry, University of Washington, Seattle, WA, USA.
A M RobitailleDepartment of Pharmacology, Howard Hughes Medical Institute, Institute for Stem Cell and Regenerative Medicine, Seattle, WA, USA.
A J ChienDepartment of Pharmacology, Howard Hughes Medical Institute, Institute for Stem Cell and Regenerative Medicine, Seattle, WA, USA.
R T MoonDepartment of Pharmacology, Howard Hughes Medical Institute, Institute for Stem Cell and Regenerative Medicine, Seattle, WA, USA.
V SherwoodSchool of Pharmacy, University of East Anglia, Norwich Research Park, Norwich, UK.
Howard Hughes Medical Institute · USNorwich Research Park · GBNinewells Hospital · GBUniversity of Washington · US

Funding

Acquisition of Embryonic Stem Cell Metabolic Signature - Minority SupplementR01GM097372 · NIGMS · UNIVERSITY OF WASHINGTON · PI RUOHOLA-BAKER, HANNELE · 2011 to 2014
$1.3M
NIGMS NIH HHS R01 GM097372
6 · The paper itself

Abstract

Aberrant regulation of WNT/β-catenin signaling has a crucial role in the onset and progression of cancers, where the effects are not always predictable depending on tumor context. In melanoma, for example, models of the disease predict differing effects of the WNT/β-catenin pathway on metastatic progression. Understanding the processes that underpin the highly context-dependent nature of WNT/β-catenin signaling in tumors is essential to achieve maximal therapeutic benefit from WNT inhibitory compounds. In this study, we have found that expression of the tumor suppressor, phosphatase and tensin homolog deleted on chromosome 10 (PTEN), alters the invasive potential of melanoma cells in response to WNT/β-catenin signaling, correlating with differing metabolic profiles. This alters the bioenergetic potential and mitochondrial activity of melanoma cells, triggered through regulation of pro-survival autophagy. Thus, WNT/β-catenin signaling is a regulator of catabolic processes in cancer cells, which varies depending on the metabolic requirements of tumors.

Indexed as

Wnt Signaling PathwayAnimalsbeta CateninHumansMaleMelanomaMiceMice, Inbred NODMice, SCIDMitochondriaPTEN Phosphohydrolasebeta CateninPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID28092677
PMCPMC5467017
OpenAlexW2578611388

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.