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. 2014 Jun 2;13:136. doi: 10.1186/1476-4598-13-136

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Copyright © 2014 Li et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), 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-I activated Akt/ERK downstream signaling pathways and induced EMT in gastric cancer cells. (A) The serum-starved MGC-803 and SGC-7901 cells were incubated with IGF-I (100 ng/mL) for the indicated times, the phosphorylation of IGF-IR, ERK and Akt were analyzed by Western blot. (B-D) The serum-starved cells were pretreated with or without OSI-906 (10 μM), PD98059 (20 μM) or LY294002 (100 μM) for 2 h followed by IGF-I (100 ng/mL) stimulation for 48 h. Cell lysates were collected for Western blot analysis. Photos were taken at × 20 magnification. E-cad, E-cadherin; OSI, OSI-906; PD, PD98059; LY, LY294002.