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Monoclonal antibody αIR‐3 inhibits non‐small cell lung cancer growth in vitro and in vivo
Author(s) -
Zia Farah,
Jacobs Steve,
Kull Frederick,
Cuttitta Frank,
Mulshine James L.,
Moody Terry W.
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240630522
Subject(s) - monoclonal antibody , in vivo , in vitro , microbiology and biotechnology , cancer research , antibody , cell culture , lung cancer , biodistribution , cell growth , biology , chemistry , immunology , medicine , pathology , biochemistry , genetics
The ability of monoclonal antibody (mAb) αI̊‐3 to interact with non‐small cell lung cancer (NSCLC) cells was investigated. MAb αI̊‐3 inhibited specific binding of 125 I‐IGF‐I and 125 I‐αI̊‐3 to a panel of 8 NSCLC cell lines with high affinity (IC 50 = 200 and 50 ng/ml, respectively). 125 I‐αI̊‐3 bound with high affinity (Kd = 40 ng/ml) to a single class of sites (Bmax = 8,000/cell) using NCI‐H838 cells. 125 I‐αI̊‐3 was internalized when exposed to NCI‐H838 or H1299 cells at 37°C but not 4°C. αI̊‐3 immunoprecipitated major 90 and 130 kD proteins. IGF‐I stimulated and αI̊‐3 inhibited the clonal growth of NCI‐H1299 cells. αI̊‐3 slowed the growth of NCI‐H157 and H838 xenografts in nude mice. In a biodistribution study 125 I‐αI̊‐3 was preferentially localized to the tumor as opposed to other organs. These data suggest that IGF‐I may be a regulatory agent in NSCLC. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.