Evidence map›Paper›PMID 31185282›Full record

ReviewSeminars in cancer biology2019

Connections between metabolism and epigenetics in cancers.

Chitra Thakur, Fei Chen

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
–field-weighted citation impact
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

98 citing papers in PubMed.

  1. Article
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  4. Review
  5. Article
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  8. Article
  9. Review
  10. Unlocking Lung Cancer Cell Dormancy: An Epigenetic Perspective.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

38 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

2 authors.

Chitra ThakurDepartment of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, 259 Mack Avenue, Detroit, MI, 48201, USA.
Fei ChenDepartment of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, 259 Mack Avenue, Detroit, MI, 48201, USA. Electronic address: fchen@wayne.edu.

Funding

Reduced Reactive Oxygen Species and Oxidative Phosphorylation in Arsenic-Induced Cancer Stem CellsR01ES028263 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2017 to 2021
$1.9M
MicroRNA-190 and Oxidative Stress in Arsenic carcinogenesisR01ES020137 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2012 to 2016
$1.7M
Mdig gene and histone demethylation in lung cancerR01ES017217 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2009 to 2013
$1.5M
Arsenic-Induced miRNA-199 and mriRNA-214 Deplete Mitochondrial DNA for the Generation of Cancer Stem-Like CellsR01ES028335 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2018 to 2022
$1.3M
NIEHS NIH HHS R01 ES017217NIEHS NIH HHS R01 ES020137NIEHS NIH HHS R01 ES028263NIEHS NIH HHS R01 ES028335
6 · The paper itself

Abstract

In the past half century, our version on cancer, from tumor initiation, growth, to metastasis, is dominated by genetic mutation. The importance of metabolism and epigenetics was not recognized until most recently. Extensive cell proliferation is one of the hallmarks of cancers. To support the energetic and anabolic demands of enhanced proliferation, tumors reprogram the pathways of nutrient procurement and metabolism. In this context, a new link between metabolic alterations and cancer progression has been unraveled over the last decade by the studies conducted in the area of cancer cell metabolism. Cancer cells are known to alter their metabolic profile during the course of tumorigenesis and metastasis thereby exhibiting a tightly regulated program of metabolic plasticity. Noteworthy, certain metabolic alteration are known to occur at the epigenetic level, thus making epigenetics and metabolism highly interwoven in a reciprocal manner. Metabolites that are generated during metabolic pathways, such as in glycolytic cycle and oxidative phosphorylation, serve as cofactors or substrates for the enzymatic reactions that catalyze the epigenetic modifications and transcriptional regulation. Several studies also indicate that the epigenome is sensitive to cellular metabolism. Since many of the metabolic alterations and consequently aberrated epigenetic regulation are common to a wide range of cancer types, they serve as promising targets for anti-cancer therapies. Here we discuss the latest findings in cancer cell metabolism, elucidating the major anabolic, catabolic and energetic demands required for sustaining cancer growth, and the influence of altered metabolism on epigenetics and vice versa. A comprehensive research pertaining to metabolomic profiling and epigenome interactors/mediators in malignant neoplasias is imperative in deciphering the potential targets that can be exploited for the development of robust anti-cancer therapies.

Indexed as

Energy MetabolismEpigenesis, GeneticGene Expression Regulation, NeoplasticAnimalsDisease SusceptibilityDNA MethylationHistonesHumansMetabolic Networks and PathwaysMolecular Targeted TherapyNeoplasmsSignal TransductionHistonesCancer cell metabolismDNA and histone methylationEpigeneticsWarburg effect

Identifiers

PMID31185282
PMCPMC6690786

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Registered trials

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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.