Evidence map›Paper›PMID 25248148›Full record

ArticlePloS one2014

A H2S-Nampt dependent energetic circuit is critical to survival and cytoprotection from damage in cancer cells.

Reiko Sanokawa-Akakura, Elena A Ostrakhovitch, Shin Akakura, Scott Goodwin, Siamak Tabibzadeh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
2.3field-weighted citation impact, top 13% 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, 38 citations in OpenAlex.

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  8. NADSignal transduction and targeted therapy · 2021
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  10. Subcellular compartmentalization of NADPharmacology & therapeutics · 2019
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  11. Exogenous HAmerican journal of physiology. Endocrinology and metabolism · 2019
    Article
  12. Review
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  14. Article
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  17. 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

5 authors at 2 institutions in 1 country.

Reiko Sanokawa-AkakuraFrontiers in Bioscience Research Institute in Aging and Cancer, Irvine, California, United States of America.
Elena A OstrakhovitchFrontiers in Bioscience Research Institute in Aging and Cancer, Irvine, California, United States of America.
Shin AkakuraFrontiers in Bioscience Research Institute in Aging and Cancer, Irvine, California, United States of America.
Scott GoodwinDept of Radiological Sciences, University of California Irvine, Irvine, California, United States of America.
Siamak TabibzadehFrontiers in Bioscience Research Institute in Aging and Cancer, Irvine, California, United States of America; Dept of Radiological Sciences, University of California Irvine, Irvine, California, United States of America.
Bioscience Research · USUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We recently demonstrated that cancer cells that recover from damage exhibit increased aerobic glycolysis, however, the molecular mechanism by which cancer cells survive the damage and show increased aerobic glycolysis remains unknown. Here, we demonstrate that diverse cancer cells that survive hypoxic or oxidative damage show rapid cell proliferation, and develop tolerance to damage associated with increased production of hydrogen sulfide (H2S) which drives up-regulation of nicotinamide phosphoribosyltransferase (Nampt). Consistent with existence of a H2S-Nampt energetic circuit, in damage recovered cancer cells, H2S, Nampt and ATP production exhibit a significant correlation. Moreover, the treatment of cancer cells with H2S donor, NaHS, coordinately increases Nampt and ATP levels, and protects cells from drug induced damage. Inhibition of cystathionine beta synthase (CBS) or cystathionase (CTH), enzymes which drive generation of H2S, decreases Nampt production while suppression of Nampt pathway by FK866, decreases H2S and ATP levels. Damage recovered cells isolated from tumors grown subcutaneously in athymic mice also show increased production of H2S, Nampt and ATP levels, associated with increased glycolysis and rapid proliferation. Together, these data show that upon recovery from potential lethal damage, H2S-Nampt directs energy expenditure and aerobic glycolysis in cancer cells, leads to their exponential growth, and causes a high degree of tolerance to damage. Identification of H2S-Nampt as a pathway responsible for induction of damage tolerance in cancer cells may underlie resistance to therapy and offers the opportunity to target this pathway as a means in treatment of cancer.

Indexed as

Energy MetabolismAcrylamidesAdenosine TriphosphateAerobiosisAnimalsCarcinoma, HepatocellularCell HypoxiaCell Line, TumorCell SurvivalCytokinesGlycolysisHumansHydrogen PeroxideHydrogen SulfideLiver NeoplasmsMaleAcrylamidesAdenosine TriphosphateCytokinesHydrogen PeroxideHydrogen SulfideN-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamideNeoplasm ProteinsNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanPiperidines

Identifiers

PMID25248148
PMCPMC4172766
OpenAlexW2048893471

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.