Molecular pathways: beta-adrenergic signaling in cancer.

摘要: β-adrenergic signaling has been found to regulate multiple cellular processes that contribute the initiation and progression of cancer, including inflammation, angiogenesis, apoptosis/anoikis, cell motility trafficking, activation tumor-associated viruses, DNA damage repair, immune response, epithelial-mesenchymal transition. In several experimental cancer models, sympathetic nervous system promotes metastasis solid epithelial tumors dissemination hematopoietic malignancies via β-adrenoreceptor-mediated PKA EPAC pathways. Within tumor microenvironment, receptors on stromal cells are activated by catecholamines from local nerve fibers (norepinephrine) circulating blood (epinephrine). Tumor-associated macrophages emerging as key targets regulation in contexts. Sympathetic biology microenvironment clarified molecular basis for long-suspected relationships between stress now suggest a highly leveraged target therapeutic intervention. Epidemiologic studies have linked use β-blockers reduced rates tumors, pre-clinical pharmacologic biomarker laying groundwork translation β-blockade novel adjuvant existing strategies clinical oncology.