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. 2014 Nov 26;7:103. doi: 10.1186/s13048-014-0103-5

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© Wang et al.; licensee BioMed Central Ltd. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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LMAb1could inhibit the proliferation of SKOV3-T. (A) LMAb1 could inhibit cell proliferation of SKOV3-T at a dose dependent manner. Similarly, the character of clone formation (B) and invasion/migration identified by transwell assay (C) could also be inhibited by LMAb1 in resistant SKOV3-T cells; (D & E) in vivo immunotherapy of LMAb1 combined with/without trastuzumab to SKOV3-T xenograft model in nude mice. D: mean tumor volume and E: overall survival rate; (F) LMAb1 could inhibit IGF-1R signal pathway transduction, for it could inhibit the MAPK and AKT activation stimulated by IGF-1. Presumably, for IGF-1R was dramatically up-regulated in acquired trastuzumab-resistant SKOV3-T cells, specific anti-IGF-1R antibody (LMAb1) could block the IGF-1R-driven signal cascade in order to help slower cell growth, reduce clone formation, shorten S-phase, and inhibit invasion and migration of cells.