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Ab-induced ectodomain shedding mediates hepatocyte growth factor receptor down-regulation and hampers biological activity.

Abstract：

:Targeting tyrosine kinase receptors (RTKs) with specific Abs is a promising therapeutic approach for cancer treatment, although the molecular mechanism(s) responsible for the Abs' biological activity are not completely known. We targeted the transmembrane RTK for hepatocyte growth factor (HGF) with a monoclonal Ab (DN30). In vitro, chronic treatment of carcinoma cell lines resulted in impairment of HGF-induced signal transduction, anchorage-independent growth, and invasiveness. In vivo, administration of DN30 inhibited growth and metastatic spread to the lung of neoplastic cells s.c. transplanted into immunodeficient nu/nu mice. This Ab efficiently down-regulates HGF receptor through a molecular mechanism involving a double proteolytic cleavage: (i) cleavage of the extracellular portion, resulting in "shedding" of the ectodomain, and (ii) cleavage of the intracellular domain, which is rapidly degraded by the proteasome. Interestingly, the "decoy effect" generated by the shed ectodomain, acting as a dominant negative molecule, enhanced the inhibitory effect of the Ab.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Petrelli A,Circosta P,Granziero L,Mazzone M,Pisacane A,Fenoglio S,Comoglio PM,Giordano S

doi

10.1073/pnas.0508156103

keywords:

subject

Has Abstract

pub_date

2006-03-28 00:00:00

pages

5090-5

issue

13

eissn

0027-8424

issn

1091-6490

pii

0508156103

journal_volume

103

pub_type

杂志文章

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