ArticleOncogene2004
Protein kinase A isozyme switching: eliciting differential cAMP signaling and tumor reversion.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
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.
Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- The importance of protein kinase A in prostate cancer: relationship to patient outcome in Radiation Therapy Oncology Group trial 92-02.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Trial
- Protein kinase A RI-alpha predicts for prostate cancer outcome: analysis of radiation therapy oncology group trial 86-10.International journal of radiation oncology, biology, physics · 2008Trial
- PKIB, a Novel Target for Cancer Therapy.International journal of molecular sciences · 2024Review
- cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment.Journal of hematology & oncology · 2024Review
- Revisiting the roles of cAMP signalling in the progression of prostate cancer.The Biochemical journal · 2023Article
- Review
- Review
- ExpressingExperimental biology and medicine (Maywood, N.J.) · 2022Article
- Complex roles of cAMP-PKA-CREB signaling in cancer.Experimental hematology & oncology · 2020Review
- Low expression of A-kinase anchor protein 5 predicts poor prognosis in non-mucin producing stomach adenocarcinoma based on TCGA data.Annals of translational medicine · 2020Article
- Article
- 8-Cl-cAMP and PKA I-selective cAMP analogs effectively inhibit undifferentiated thyroid cancer cell growth.Endocrine · 2017Article
- A2A adenosine receptor antagonists to weaken the hypoxia-HIF-1α driven immunosuppression and improve immunotherapies of cancer.Current opinion in pharmacology · 2016Review
- Regulation of Cancer Cell Behavior by the Small GTPase Rab13.The Journal of biological chemistry · 2016Review
- PKA-type I selective constrained peptide disruptors of AKAP complexes.ACS chemical biology · 2015Article
- PKA signaling drives mammary tumorigenesis through Src.Oncogene · 2015Article
- Targeting protein kinase A in cancer therapy: an update.EXCLI journal · 2014Review
- Implementing fluorescence anisotropy screening and crystallographic analysis to define PKA isoform-selective activation by cAMP analogs.ACS chemical biology · 2013Article
- Cyclic AMP and c-KIT signaling in familial testicular germ cell tumor predisposition.The Journal of clinical endocrinology and metabolism · 2013Article
- A-kinase anchoring proteins 10 expression in relation to 2073A/G polymorphism and tumor progression in patients with colorectal cancer.Pathology oncology research : POR · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The cAMP-dependent protein kinase types I (PKA-I) and II (PKA-II), composed of identical catalytic (C) subunits but distinct regulatory (R) subunits (RI versus RII), are expressed in a balance of cell growth and differentiation. Distortion of this balance may underlie tumorigenesis and tumor growth. Here, we used PC3M prostate carcinoma cells as a model to overexpress wild type and mutant R and C subunit genes and examined the effects of differential expression of these genes on tumor growth. Only the RIIbeta and mutant RIalpha-P (a functional mimic of RIIbeta) transfectants exhibited growth inhibition in vitro, reverted phenotype, and apoptosis, and inhibited in vivo tumor growth. DNA microarrays demonstrated that RIIbeta and RIalpha-P overexpression upregulated a cluster of differentiation genes, while downregulating transformation and proliferation signatures. Overexpression of RIalpha and Calpha, which upregulated PKA-I, elicited the expression signatures opposite that elicited by RIIbeta overexpression. Total colocalization of Calpha and RIIbeta seen by confocal microscopy in the RIIbeta cell nucleus supports the opposed genomic regulation demonstrated between Calpha and RIIbeta cells. Differential expression of PKA R subunits may therefore serve as a tumor-target-based gene therapy for PC3M prostate and other cancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.