Abstract
Our previous study demonstrated that Angiotensin II (Ang-II) which is well known to be a main peptide of the renin-angiotensin system could activate the cell proliferation of prostate cancer as well as EGF, and an Ang-II receptor blocker(ARB) could inhibit it through the suppression of phosphorylation of MAPK and STAT3. Also, ARB exerted an antiproliferative effect on prostate cancer through paracrine factors from stromal cells. We believe that ARBs have the novel ability to suppress the development or progression of prostate cancer. Furthermore, based on the idea that inhibition of G protein-coupled receptor signaling in cancer and stromal cells could suppress prostate cancer growth, a novel treatment such as molecular targeting therapy to overcome this devastating disease could be possible in the future.
MeSH terms
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Angiotensin II / physiology
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Angiotensin II Type 1 Receptor Blockers / pharmacology
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Angiotensin II Type 1 Receptor Blockers / therapeutic use*
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Cell Division / drug effects
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Cytokines / metabolism
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DNA-Binding Proteins / metabolism
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Depression, Chemical
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Humans
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Male
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Phosphorylation / drug effects
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Prostatic Neoplasms / drug therapy*
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Prostatic Neoplasms / metabolism
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Prostatic Neoplasms / pathology
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Quality of Life
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Receptors, G-Protein-Coupled / antagonists & inhibitors
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STAT3 Transcription Factor
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Signal Transduction / drug effects
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Trans-Activators / metabolism
Substances
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Angiotensin II Type 1 Receptor Blockers
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Cytokines
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DNA-Binding Proteins
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Receptors, G-Protein-Coupled
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STAT3 Transcription Factor
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STAT3 protein, human
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Trans-Activators
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Angiotensin II
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Extracellular Signal-Regulated MAP Kinases