Evidence map›Paper›PMID 23940778›Full record

ArticlePloS one2013

Proteomic analysis of signaling network regulation in renal cell carcinomas with differential hypoxia-inducible factor-2α expression.

Lokesh Dalasanur Nagaprashantha, Tatjana Talamantes, Jyotsana Singhal, Jia Guo, Rit Vatsyayan, Navin Rauniyar, Sanjay Awasthi, Sharad S Singhal, Laszlo Prokai

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Label-free quantitative proteomic analysis reveals potential biomarkers and pathways in renal cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  5. 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

9 authors at 2 institutions in 1 country.

Lokesh Dalasanur NagaprashanthaDepartment of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas, United States of America.
Tatjana Talamantes
Jyotsana Singhal
Jia Guo
Rit Vatsyayan
Navin Rauniyar
Sanjay Awasthi
Sharad S Singhal
Laszlo Prokai
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

MECHANISM OF DRUG TRANSPORT IN LUNG CANCER CELLSR01CA077495 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI AWASTHI, SANJAY · 1998 to 2011
$2.8M
NCI NIH HHS CA077495NCI NIH HHS R01 CA077495
6 · The paper itself

Abstract

backgroundThe loss of von Hippel-Lindau (VHL) protein function leads to highly vascular renal tumors characterized by an aggressive course of disease and refractoriness to chemotherapy and radiotherapy. Loss of VHL in renal tumors also differs from tumors of other organs in that the oncogenic cascade is mediated by an increase in the levels of hypoxia-inducible factor-2α (HIF2α) instead of hypoxia-inducible factor-1α (HIF1α). METHODS AND PRINCIPAL

findingsWe used renal carcinoma cell lines that recapitulate the differences between mutant VHL and wild-type VHL genotypes. Utilizing a method relying on extracted peptide intensities as a label-free approach for quantitation by liquid chromatography-mass spectrometry, our proteomics study revealed regulation of key proteins important for cancer cell survival, proliferation and stress-resistance, and implicated differential regulation of signaling networks in VHL-mutant renal cell carcinoma. We also observed upregulation of cellular energy pathway enzymes and the stress-responsive mitochondrial 60-kDa heat shock protein. Finding reliance on glutaminolysis in VHL-mutant renal cell carcinoma was of particular significance, given the generally predominant dependence of tumors on glycolysis. The data have been deposited to the ProteomeXchange with identifier PXD000335. CONCLUSIONS AND SIGNIFICANCE: Pathway analyses provided corroborative evidence for differential regulation of molecular and cellular functions influencing cancer energetics, metabolism and cell proliferation in renal cell carcinoma with distinct VHL genotype. Collectively, the differentially regulated proteome characterized by this study can potentially guide translational research specifically aimed at effective clinical interventions for advanced VHL-mutant, HIF2α-over-expressing tumors.

Indexed as

Metabolic Networks and PathwaysBasic Helix-Loop-Helix ProteinsCarcinoma, Renal CellCell Line, TumorEndothelial PAS Domain-Containing Protein 1Gene Expression Regulation, NeoplasticHumansKidney NeoplasmsMutationProteomeProteomicsSignal TransductionVon Hippel-Lindau Tumor Suppressor ProteinBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1ProteomeVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID23940778
PMCPMC3733962
OpenAlexW1975508870

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.