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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
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Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
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GPCR Desensitization

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G-Protein Gated Ion Channels

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Heart Failure Drugs: Inotropic Agents

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MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent
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MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent

Published on: September 3, 2013

Cardiac glycosides decrease prostate specific antigen expression by down-regulation of prostate derived Ets factor.

Horng-Heng Juang1, Yu-Fen Lin, Phei-Lang Chang

  • 1Department of Anatomy, Chang Gung University, Kwei-Shan, Taiwan, Republic of China.

The Journal of Urology
|September 21, 2010
PubMed
Summary
This summary is machine-generated.

Cardiac glycosides, like digoxin and digitoxin, inhibit prostate specific antigen (PSA) secretion and gene expression in prostate cancer cells. This effect is linked to reduced prostate derived Ets factor, suggesting a potential therapeutic avenue for prostate cancer.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Pharmacology

Background:

  • Cardiac glycosides are established treatments for heart failure.
  • Previous research indicated cardiac glycosides can inhibit prostate cancer cell proliferation.
  • The precise mechanisms of this inhibition, particularly on prostate specific antigen (PSA) gene expression, require further elucidation.

Purpose of the Study:

  • To investigate the effects of cardiac glycosides (digoxin, digitoxin, ouabain) on prostate specific antigen (PSA) gene expression in vitro.
  • To explore the underlying mechanisms by which cardiac glycosides influence PSA expression in prostate cancer cells.

Main Methods:

  • LNCaP cells were cultured to assess the impact of cardiac glycosides.
  • Prostate specific antigen (PSA) and prostate derived Ets factor expression were analyzed using reverse transcription-polymerase chain reaction, immunoblot, transient gene expression assays, and enzyme-linked immunosorbent assay.
  • The effects of noncytotoxic and chronic low-dose treatments were evaluated.

Main Results:

  • Noncytotoxic doses (100 nM) of cardiac glycosides significantly inhibited PSA secretion and down-regulated PSA and prostate derived Ets factor expression in LNCaP cells.
  • Cardiac glycosides attenuated the promoter activity of both PSA and prostate derived Ets factor genes.
  • Chronic treatment (60 hours) with digitoxin or digoxin at 25 nM reduced PSA secretion by 30%.

Conclusions:

  • Cardiac glycosides inhibit PSA gene expression, potentially through the down-regulation of prostate derived Ets factor.
  • Chronic exposure to therapeutic concentrations of digoxin or digitoxin led to decreased PSA secretion.
  • These findings warrant further investigation into the clinical relevance for men undergoing cardiac glycoside therapy.