Evidence map›Paper›PMID 18723829›Full record

ArticleMolecular cancer research : MCR2008

SIRT1 contributes in part to cisplatin resistance in cancer cells by altering mitochondrial metabolism.

Xing-Jie Liang, Toren Finkel, Ding-Wu Shen, Jun-Jie Yin, Adorjan Aszalos, Michael M Gottesman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

70 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  8. Forkhead box O proteins: steering the course of stem cell fate.Cell regeneration (London, England) · 2024
    Review
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  18. Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration.International journal of molecular sciences · 2021
    Review
  19. Article
  20. Article

10 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

6 authors at 3 institutions in 3 countries.

Xing-Jie LiangLaboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA. liangxj@nanoctr.cn
Toren Finkel
Ding-Wu Shen
Jun-Jie Yin
Adorjan Aszalos
Michael M Gottesman
National Cancer Institute · MYCenter for Food Safety and Applied Nutrition · USNational Heart Lung and Blood Institute · US

Funding

Mechanisms of non-classical multidrug resistance in cancerZIABC010830 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GOTTESMAN, MICHAEL · 2009 to 2025
$19.6M
The role of autophagy in aging and metabolismZIAHL005012 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 2009 to 2017
$11.8M
Reactive Oxygen Species, Stem cells and AgingZ01HL005012 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 1997 to 2008
$5.5M
Mechanisms of non-classical multidrug resistance in cancerZ01BC010830 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GOTTESMAN, MICHAEL · 2007 to 2008
$1.3M
Intramural NIH HHS Z01 BC010830Intramural NIH HHS Z01 HL005012
6 · The paper itself

Abstract

Tumors frequently develop resistance to cisplatin, a platinum drug used as a cornerstone of present-day chemotherapy regimens, significantly decreasing its usefulness in the clinic. Although it is known that cisplatin-resistant (CP-r) cancer cells commonly grow more slowly and exhibit reduced uptake of various compounds, including nutrients, the effect of tumor metabolism on cisplatin resistance is unclear. It was found that in CP-r cells, uptake of 2-deoxyglucose was reduced due to dysfunction and altered morphology of mitochondria compared with cisplatin-sensitive parental cancer cells. The CP-r cells overexpressed SIRT1, a histone deacetylase that plays a central role in DNA damage response and transcriptional silencing. Incubation of drug-sensitive cells in low glucose medium induced the expression of SIRT1 and increased cellular resistance to cisplatin. Reduced SIRT1 expression by a SIRT1 SMART small interfering RNA duplex sensitized the >20-fold resistant CP-r cells to cisplatin treatment 1.5- to 2-fold, and SIRT1 overexpression by SIRT1 cDNA transfection increased cisplatin resistance in cisplatin-sensitive cells by 2- to 3-fold. Our findings therefore suggest that reduced glucose use and altered mitochondrial metabolism mediated by SIRT1 is one of several alterations that contribute to cellular resistance to cisplatin.

Indexed as

Drug Resistance, NeoplasmAdenocarcinomaAntineoplastic AgentsCarcinoma, HepatocellularCarcinoma, Squamous CellCell SurvivalCellular StructuresCisplatinDeoxyglucoseElectron Spin Resonance SpectroscopyFlow CytometryFluorescent Antibody TechniqueHumansImmunoblottingLiver NeoplasmsMembrane Potential, MitochondrialAntineoplastic AgentsCisplatinDeoxyglucoseRNA, Small InterferingSIRT1 protein, humanSirtuin 1Sirtuins

Identifiers

PMID18723829
PMCPMC2597364
OpenAlexW2130503166

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.