Evidence map›Paper›PMID 21637840›Full record

ArticlePloS one2011

Quantitative proteomic and interaction network analysis of cisplatin resistance in HeLa cells.

Juan D Chavez, Michael R Hoopmann, Chad R Weisbrod, Kohji Takara, James E Bruce

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Contemporary insights into elamipretide's mitochondrial mechanism of action and therapeutic effects.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Mitochondrial protein interaction landscape of SS-31.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular mechanisms of cisplatin resistance in cervical cancer.Drug design, development and therapy · 2016
    Review
  16. Article
  17. Article
  18. Review
  19. 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

5 authors at 2 institutions in 2 countries.

Juan D ChavezDepartment of Genome Sciences, University of Washington, Seattle, Washington, United States of America.
Michael R Hoopmann
Chad R Weisbrod
Kohji Takara
James E Bruce
University of Washington · USHimeji Dokkyo University · JP

Funding

Quantitation of protein interactions in cancer cellsR01GM086688 · NIGMS · UNIVERSITY OF WASHINGTON · PI BRUCE, JAMES EDWARD · 2009 to 2019
$4.2M
An LC-FTICR Mass Spectrometer for Proteomics and Metabolomics ResearchS10RR025107 · NCRR · UNIVERSITY OF WASHINGTON · PI BRUCE, JAMES EDWARD · 2008 to 2008
$990k
New Technology for Protein Interaction Network and Topology AnalysisR01RR023334 · NCRR · WASHINGTON STATE UNIVERSITY · PI BRUCE, JAMES EDWARD · 2007 to 2009
$750k
NCRR NIH HHS R01 RR023334NCRR NIH HHS R01RR023334NCRR NIH HHS S10 RR025107NCRR NIH HHS S10RR025107NIGMS NIH HHS R01 GM086688NIGMS NIH HHS R01GM086688
6 · The paper itself

Abstract

Cisplatin along with other platinum based drugs are some of the most widely used chemotherapeutic agents. However drug resistance is a major problem for the successful chemotherapeutic treatment of cancer. Current evidence suggests that drug resistance is a multifactorial problem due to changes in the expression levels and activity of a wide number of proteins. A majority of the studies to date have quantified mRNA levels between drug resistant and drug sensitive cell lines. Unfortunately mRNA levels do not always correlate with protein expression levels due to post-transcriptional changes in protein abundance. Therefore global quantitative proteomics screens are needed to identify the protein targets that are differentially expressed in drug resistant cell lines. Here we employ a quantitative proteomics technique using stable isotope labeling with amino acids in cell culture (SILAC) coupled with mass spectrometry to quantify changes in protein levels between cisplatin resistant (HeLa/CDDP) and sensitive HeLa cells in an unbiased fashion. A total of 856 proteins were identified and quantified, with 374 displaying significantly altered expression levels between the cell lines. Expression level data was then integrated with a network of protein-protein interactions, and biological pathways to obtain a systems level view of proteome changes which occur with cisplatin resistance. Several of these proteins have been previously implicated in resistance towards platinum-based and other drugs, while many represent new potential markers or therapeutic targets.

Indexed as

Blotting, WesternCisplatinDrug Resistance, NeoplasmHeLa CellsHumansNeoplasm ProteinsProtein BindingProteomicsSignal TransductionCisplatinNeoplasm Proteins

Identifiers

PMID21637840
PMCPMC3102677
OpenAlexW2028375501

What OpenQuestion holds

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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.