Selective β2-AR Blockage Suppresses Colorectal Cancer Growth Through Regulation of EGFR-Akt/ERK1/2 Signaling, G1-Phase Arrest, and Apoptosis.

摘要: Abstract The stress-upregulated catecholamines-activated β1- and β2-adrenergic receptors (β1/2-ARs) have been shown to accelerate the progression of cancers such as colorectal cancer (CRC). We investigated underlying mechanism inhibition β1/2-ARs signaling for treatment CRC elucidated significance β2-AR expression in vitro clinical samples. impacts β1/2-AR antagonists CRC-xenograft vivo were examined. found that repression but not β1-AR selectively suppressed cell viability, induced G1-phase cycle arrest, caused both intrinsic extrinsic pathways-mediated apoptosis specific cells inhibited growth vivo. Moreover, was consistent with or Our data evidence profiles, signaling, blockage a unique pattern comparing other cancers. antagonism suppresses accompanying active which potentially carries wild-type KRAS, via transactivated EFGR-Akt/ERK1/2 pathway. Thus, might be potential therapeutic strategy combating progressions β2-AR-dependent CRC. J. Cell. Physiol. 231: 459-472, 2016. © 2015 Wiley Periodicals, Inc.