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Front Oncol. 2015 Jan 12;4:375. doi: 10.3389/fonc.2014.00375. eCollection 2014.

β-Adrenergic Receptor Signaling in Prostate Cancer.

Author information

1
Department of Tumor Biology, Institute of Cancer Research, Division of Cancer Medicine, Transplantation and Surgery, Oslo University Hospital , Oslo , Norway.
2
Department of Tumor Biology, Institute of Cancer Research, Division of Cancer Medicine, Transplantation and Surgery, Oslo University Hospital , Oslo , Norway ; Institute of Clinical Medicine, University of Oslo , Oslo , Norway.

Abstract

Enhanced sympathetic signaling, often associated with obesity and chronic stress, is increasingly acknowledged as a contributor to cancer aggressiveness. In prostate cancer, intact sympathetic nerves are critical for tumor formation, and sympathectomy induces apoptosis and blocks tumor growth. Perineural invasion, involving enrichment of intra-prostatic nerves, is frequently observed in prostate cancer and is associated with poor prognosis. β2-adrenergic receptor (ADRB2), the most abundant receptor for sympathetic signals in prostate luminal cells, has been shown to regulate trans-differentiation of cancer cells to neuroendocrine-like cells and to affect apoptosis, angiogenesis, epithelial-mesenchymal transition, migration, and metastasis. Epidemiologic studies have shown that use of β-blockers, inhibiting β-adrenergic receptor activity, is associated with reduced prostate cancer-specific mortality. In this review, we aim to present an overview on how β-adrenergic receptor and its downstream signaling cascade influence the development of aggressive prostate cancer, primarily through regulating neuroendocrine differentiation.

KEYWORDS:

ADRB2; angiogenesis; apoptosis; metastasis; neuroendocrine differentiation; prostate cancer; β-adrenergic receptor; β-blocker

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