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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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IGF-1R can promote the proliferation of SKOV3. (A) IGF-1R expression was up-regulated in SKOV3-T while HER2 was opposite by flow cytometry analysis; (B) IGF-1R-positive SKOV3 cell preparation by eukaryotic transfection with pCMV6-IGF-1R plasmid. Cell proliferation (C) and agar clone formation (D) assays both indicated the enhanced carcinogenic activity of IGF-1R-positive SKOV3 cells, while according to cell cycle analysis (E), SKOV3-IGF1R owned more S-phase cells in order to multiply quicker; Similarly, in vivo tumor model (F) further displayed more rapid tumor growth of SKOV3-IGF1R, indicating that IGF-1R can promote the cell survival and multiplication in ovarian cancer SKOV3 cells. To be clear, in this figure, “SKOV3” sample means original pCMV6 transfected cells.