Evidence map›Paper›PMID 24583643›Full record

ArticleCell death and differentiation2014

RIP1 maintains DNA integrity and cell proliferation by regulating PGC-1α-mediated mitochondrial oxidative phosphorylation and glycolysis.

W Chen, Q Wang, L Bai, W Chen, X Wang, C S Tellez, S Leng, M T Padilla, T Nyunoya, S A Belinsky and 1 more

Abstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Inhibition of glycolytic reprogramming suppresses innate immune-mediated inflammation in experimental amyotrophic lateral sclerosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Storage Primes Erythrocytes for Necroptosis and Clearance.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019
    Article
  17. Review
  18. Review
  19. Metabolic reprogramming during neuronal differentiation.Cell death and differentiation · 2016
    Article
  20. 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

11 authors.

W ChenMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
Q Wang1] Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA [2] Laboratory of Molecular and Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education at Sichuan University, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, China.
L BaiMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
W ChenMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
X Wang1] Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA [2] Laboratory of Molecular and Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education at Sichuan University, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, China.
C S TellezMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
S LengMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
M T PadillaMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
T NyunoyaMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
S A BelinskyMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.
Y LinMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest DR. SE, Albuquerque, NM, USA.

Funding

Bridging Inflammation and Cigarette Smoke-associated Lung Carcinogenesis by MUC1R01ES017328 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2010 to 2014
$2.2M
Lung Cancer Prevention by Quercetin Through IL-6 Secretion & SignalingR03CA167727 · NCI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI CHEN, WENSHU · 2013 to 2014
$213k
NCI NIH HHS R03 CA167727NCI NIH HHS R03CA167727NIEHS NIH HHS R01 ES017328NIEHS NIH HHS R01ES017328
6 · The paper itself

Abstract

Aerobic glycolysis or the Warburg effect contributes to cancer cell proliferation; however, how this glucose metabolism pathway is precisely regulated remains elusive. Here we show that receptor-interacting protein 1 (RIP1), a cell death and survival signaling factor, regulates mitochondrial oxidative phosphorylation and aerobic glycolysis. Loss of RIP1 in lung cancer cells suppressed peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) expression, impairing mitochondrial oxidative phosphorylation and accelerating glycolysis, resulting in spontaneous DNA damage and p53-mediated cell proliferation inhibition. Thus, although aerobic glycolysis within a certain range favors cancer cell proliferation, excessive glycolysis causes cytostasis. Our data suggest that maintenance of glycolysis by RIP1 is pivotal to cancer cell energy homeostasis and DNA integrity and may be exploited for use in anticancer therapy.

Indexed as

Cell ProliferationAnimalsCell Line, TumorDNA DamageGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlycolysisHumansMice, NudeMitochondriaNeoplasm TransplantationNuclear Pore Complex ProteinsOxidative PhosphorylationPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRNA-Binding ProteinsTranscription FactorsAGFG1 protein, humanNuclear Pore Complex ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanRNA-Binding ProteinsTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID24583643
PMCPMC4207474

What OpenQuestion holds

Textmetadata
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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.