Evidence map›Paper›PMID 25677747›Full record

ArticleBreast cancer research and treatment2015

Targeting metabolic plasticity in breast cancer cells via mitochondrial complex I modulation.

Qijin Xu, Eva Biener-Ramanujan, Wei Yang, V Krishnan Ramanujan

Abstract read
In one paragraph

Article in Breast cancer research and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Antioxidant functions of DHHC3 suppress anti-cancer drug activities.Cellular and molecular life sciences : CMLS · 2021
    Article
  7. Review
  8. Rapid Assessment of Mitochondrial Complex I Activity and Metabolic Phenotyping of Breast Cancer Cells by NAD(p)H Cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. The Mitochondrial Complex(I)ty of Cancer.Frontiers in oncology · 2017
    Review
  13. Article
  14. Article
  15. Review
  16. Direct measurement of catalase activity in living cells and tissue biopsies.Biochemical and biophysical research communications · 2016
    Article
  17. Article
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

4 authors at 1 institution in 1 country.

Qijin XuMetabolic Photonics Laboratory, Department of Surgery, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA, 90048, USA, xuq@cshs.org.
Eva Biener-Ramanujan
Wei Yang
V Krishnan Ramanujan
Cedars-Sinai Medical Center · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Multiphoton Fluorescence Lifetime Imaging of Solid Tumors InvivoR21CA124843 · NCI · CEDARS-SINAI MEDICAL CENTER · PI RAMANUJAN, V.KRISHNAN · 2009 to 2010
$378k
NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NCI NIH HHS R21 CA124843NCI NIH HHS R21-CA124843
6 · The paper itself

Abstract

Heterogeneity commonly observed in clinical tumors stems both from the genetic diversity as well as from the differential metabolic adaptation of multiple cancer types during their struggle to maintain uncontrolled proliferation and invasion in vivo. This study aims to identify a potential metabolic window of such adaptation in aggressive human breast cancer cell lines. With a multidisciplinary approach using high-resolution imaging, cell metabolism assays, proteomic profiling and animal models of human tumor xenografts and via clinically-relevant pharmacological approach for modulating mitochondrial complex I function in human breast cancer cell lines, we report a novel route to target metabolic plasticity in human breast cancer cells. By a systematic modulation of mitochondrial function and by mitigating metabolic switch phenotype in aggressive human breast cancer cells, we demonstrate that the resulting metabolic adaptation signatures can predictably decrease tumorigenic potential in vivo. Proteomic profiling of the metabolic adaptation in these cells further revealed novel protein-pathway interactograms highlighting the importance of antioxidant machinery in the observed metabolic adaptation. Improved metabolic adaptation potential in aggressive human breast cancer cells contribute to improving mitochondrial function and reducing metabolic switch phenotype-which may be vital for targeting primary tumor growth in vivo.

Indexed as

Adaptation, PhysiologicalAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationDisease Models, AnimalElectron Transport Complex IFemaleHeterograftsHumansMetabolic Networks and PathwaysMiceMitochondriaOxidation-ReductionProteomeProteomicsElectron Transport Complex IProteomeRotenoneUncoupling Agents

Identifiers

PMID25677747
PMCPMC5127648
OpenAlexW2157796965

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.