Home CONTACT Neoplasma 2009 Neoplasma Vol.56, No.2, p.108-113, 2009

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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Neoplasma Vol.56, No.2, p.108-113, 2009

Title: β-arrestin2 inhibits opioid-induced breast cancer cell death through Akt and caspase-8 pathways
Author: M. Zhao, G. Zhou, Y. Zhang, T. Chen, X. Sun, C. Stuart, G. Hanley, J. Li, J. Zhang, D. Yin

Abstract: β-arrestins, a family of regulatory and scaffold proteins, are well-known negative regulators of G-protein-coupled receptors (GPCRs) including opioid receptors. Recent studies have shown that β-arrestin2 plays a potential role in inhibiting cell death. It has been reported that opioids such as morphine induce cell death at high concentrations (>500 µM for 24 hours), which is similar to morphine plasma concentrations in cancer patients receiving chronic morphine treatment for pain relievers. However, the role of β-arrestin2 in opioid-induced cell death remains to be elucidated. We report here that β-arrestin2 significantly blocks morphine-induced number of cell death in human breast cancer MCF-7 and MDA-MB231 cells. Suppression of endogenous β-arrestin2 by specific RNA interfering (RNAi) and morphine treatment significantly attenuates the levels of phosphorylated Akt compared with inhibition of β-arrestin2 or morphine treatment alone. However, blockade of morphine-induced cell death by β-arrestin2 seems to be dependent on the inhibition of caspase-8, as inhibition of β-arrestin2 and morphine treatment significantly enhanced the levels of cleaved caspase-8. These studies show for the first time that β-arrestin2 blocks morphine-induced cell death through anti-apoptotic Akt and pro-apoptotic caspase-8 pathways. Therefore, targeting β-arrestin2 may be useful for treating side effects of opioids as pain relievers for cancer patients.

Keywords: Breast cancer, β-arrestin, opioid. Akt, caspase-8,cell death
Year: 2009, Volume: 56, Issue: 2 Page From: 108, Page To: 113
doi:10.4149/neo_2009_02_108
Price: 14.40 €






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