Evidence map›Paper›PMID 28596418›Full record

ArticleMolecular cancer research : MCR2017

ERRα Maintains Mitochondrial Oxidative Metabolism and Constitutes an Actionable Target in PGC1α-Elevated Melanomas.

Chi Luo, Eduardo Balsa, Ajith Thomas, Maximilian Hatting, Mark Jedrychowski, Steven P Gygi, Hans R Widlund, Pere Puigserver

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  9. Targeting PGC1α to wrestle cancer: a compelling therapeutic opportunity.Journal of cancer research and clinical oncology · 2022
    Review
  10. Article
  11. Connecting Metabolic Rewiring With Phenotype Switching in Melanoma.Frontiers in cell and developmental biology · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Repression of the transcriptional activity of ERRα with sequence-specific DNA-binding polyamides.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2020
    Article
  18. Article
  19. Review
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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

8 authors at 1 institution in 1 country.

Chi LuoDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Eduardo BalsaDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Ajith ThomasDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Maximilian HattingDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Mark JedrychowskiDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts.
Steven P GygiDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts.
Hans R WidlundBrigham and Women's Hospital, Department of Dermatology, Harvard Medical School, Boston, Massachusetts.
Pere PuigserverDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts. Pere_Puigserver@dfci.harvard.edu.
Harvard University · US

Funding

Metabolic Vulnerabilities in Melanoma TumorsR01CA181217 · NCI · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2014 to 2024
$3.7M
NCI NIH HHS R01 CA181217
6 · The paper itself

Abstract

The uncontrolled growth of tumors provides metabolic dependencies that can be harnessed for therapeutic benefit. Although tumor cells exhibit these increased metabolic demands due to their rapid proliferation, these metabolic processes are general to all cells, and furthermore, targeted therapeutic intervention can provoke compensatory adaptation that alters tumors' characteristics. As an example, a subset of melanomas depends on the transcriptional coactivator PGC1α function to sustain their mitochondrial energy-dependent survival. However, selective outgrowth of resistant PGC1α-independent tumor cells becomes endowed with an augmented metastatic phenotype. To find PGC1α-dependent components that would not affect metastasis in melanomas, an unbiased proteomic analyses was performed and uncovered the orphan nuclear receptor ERRα, which supports PGC1α's control of mitochondrial energetic metabolism, but does not affect the antioxidant nor antimetastatic regulatory roles. Specifically, genetic or pharmacologic inhibition of ERRα reduces the inherent bioenergetic capacity and decreases melanoma cell growth, but without altering the invasive characteristics. Thus, within this particularly aggressive subset of melanomas, which is characterized by heighted expression of PGC1α, ERRα specifically mediates prosurvival functions and represents a tangible therapeutic target.

Indexed as

AnimalsCell Line, TumorERRalpha Estrogen-Related ReceptorHumansMelanomaMiceMitochondriaNeoplasm TransplantationOxidative PhosphorylationOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProteomicsReceptors, EstrogenERRalpha Estrogen-Related ReceptorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanReceptors, Estrogen

Identifiers

PMID28596418
PMCPMC5954239
OpenAlexW2622177359

What OpenQuestion holds

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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.