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脑啡肽刺激白血病细胞迁移及CD9的表面表达。

Enkephalins stimulate leukemia cell migration and surface expression of CD9.

作者信息

Heagy W, Duca K, Finberg R W

机构信息

Laboratory of Infectious Diseases, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

出版信息

J Clin Invest. 1995 Sep;96(3):1366-74. doi: 10.1172/JCI118171.

Abstract

Opioid peptides have been implicated in the regulation of tumor growth and biology; however, little attention has been given to the mechanisms that are involved. In this study we show that physiological concentrations of the endogenous opioid neuropeptide methionine-enkephalin (MET-ENK) and the synthetic enkephalins D-Ala2, Me-Phe4, Gly(ol)5 and D-Ala2, D-Leu5 are stimulants for the in vitro migration of pre-B acute lymphoblastoid leukemia (ALL) cells. Activation of the human pre-B ALL cell lines NALM 6 and LAZ 221 with MET-ENK resulted in both an increase in their migration and an augmentation in the surface expression of the leukemia cell marker CD9. The opiate receptor antagonist naloxone reversed these enkephalin-induced effects on the leukemia cells. When the pre-B ALL cells were preincubated with an anti-CD9 mAb before challenge with MET-ENK their migration to the enkephalin was markedly reduced. These studies show that endogenous and synthetic opioid peptides are stimulants for pre-B ALL cell migration and suggest that CD9 is important in the regulation of leukemia cell motility.

摘要

阿片肽与肿瘤生长和生物学调节有关;然而,对其中涉及的机制却鲜有关注。在本研究中,我们发现内源性阿片神经肽甲硫氨酸脑啡肽(MET-ENK)以及合成脑啡肽D-Ala2、Me-Phe4、Gly(ol)5和D-Ala2、D-Leu5的生理浓度可刺激前B急性淋巴细胞白血病(ALL)细胞的体外迁移。用MET-ENK激活人前B ALL细胞系NALM 6和LAZ 221,导致其迁移增加以及白血病细胞标志物CD9的表面表达增强。阿片受体拮抗剂纳洛酮可逆转这些脑啡肽诱导的对白血病细胞的作用。当用抗CD9单克隆抗体对前B ALL细胞进行预孵育,然后再用MET-ENK刺激时,它们向脑啡肽的迁移明显减少。这些研究表明,内源性和合成阿片肽是前B ALL细胞迁移的刺激物,并提示CD9在白血病细胞运动性调节中很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc28/185758/9486a35c2842/jcinvest00015-0200-a.jpg

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