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Research Article Free access | 10.1172/JCI118171

Enkephalins stimulate leukemia cell migration and surface expression of CD9.

W Heagy, K Duca, and R W Finberg

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

Find articles by Heagy, W. in: PubMed | Google Scholar

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

Find articles by Duca, K. in: PubMed | Google Scholar

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

Find articles by Finberg, R. in: PubMed | Google Scholar

Published September 1, 1995 - More info

Published in Volume 96, Issue 3 on September 1, 1995
J Clin Invest. 1995;96(3):1366–1374. https://doi.org/10.1172/JCI118171.
© 1995 The American Society for Clinical Investigation
Published September 1, 1995 - Version history
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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.

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