Evidence map›Paper›PMID 10639166›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Extracellular protein kinase A as a cancer biomarker: its expression by tumor cells and reversal by a myristate-lacking Calpha and RIIbeta subunit overexpression.

Y S Cho, Y G Park, Y N Lee, M K Kim, S Bates, L Tan, Y S Cho-Chung

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

33 citing papers in PubMed, 116 citations in OpenAlex.

  1. Anticancer Effects ofLife (Basel, Switzerland) · 2024
    Article
  2. Opportunities and Challenges of Kava in Lung Cancer Prevention.International journal of molecular sciences · 2023
    Review
  3. Article
  4. Review
  5. Protein Kinase A Detection in Human Urine Samples.Journal of clinical medicine · 2021
    Article
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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

7 authors at 2 institutions in 1 country.

Y S ChoCellular Biochemistry Section, Laboratory of Tumor Immunology and Biology, National Institutes of Health, National Cancer Institute, Bethesda, MD 20892-1750, USA.
Y G Park
Y N Lee
M K Kim
S Bates
L Tan
Y S Cho-Chung
National Institutes of Health · USNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of cAMP-dependent protein kinase (PKA) type I isozyme is associated with cell proliferation and neoplastic transformation. The presence of PKA on the external surface of LS-174T human colon carcinoma cells has been shown. Here, we show that cancer cells of various cell types excrete PKA into the conditioned medium. This extracellular PKA (ECPKA) is present in active, free catalytic subunit (C subunit) form, and its activity is specifically inhibited by PKA inhibitory protein, PKI. Overexpression of the Calpha or RIalpha subunit gene of PKA in an expression vector, which up-regulates intracellular PKA type I, markedly up-regulates ECPKA expression. In contrast, overexpression of the RIIbeta subunit, which eliminates PKA type I, up-regulates PKA type II, and reverts the transformed phenotype, down-regulates ECPKA. A mutation in the Calpha gene that prevents myristylation allows the intracellular PKA up-regulation but blocks the ECPKA increase, suggesting that the NH(2)-terminal myristyl group of Calpha is required for the ECPKA expression. In serum of cancer patients, the ECPKA expression is up-regulated 10-fold as compared with normal serum. These results indicate that the ECPKA expression is an ordered cellular response of a living cell to actively exclude excess intracellular PKA molecules from the cell. This phenomenon is up-regulated in tumor cells and has an inverse relationship with the hormone dependency of breast cancer. Thus, the extracellular PKA may serve as a potential diagnostic and prognostic marker for cancer.

Indexed as

3T3 CellsAnimalsBiomarkers, TumorBreast NeoplasmsCell LineCell Transformation, NeoplasticCulture Media, ConditionedCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP-Dependent Protein Kinase Type IIExtracellular SpaceGene Expression Regulation, EnzymologicHormonesHumansIsoenzymesMiceBiomarkers, TumorCulture Media, ConditionedCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP-Dependent Protein Kinase Type IIHormonesIsoenzymesMyristic AcidProstate-Specific AntigenRecombinant Fusion Proteins

Identifiers

PMID10639166
PMCPMC15417
OpenAlexW1974985535

What OpenQuestion holds

Textmetadata
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.