Fujimoto et al. BMC Cancer 2010, 10:443 http://www.biomedcentral.com/1471-2407/10/443 Page 5 of 14 Figure 2 Proliferation assay in MKN45/Mock. This figure showed that the MKN45/mock (1.0×104 cells/well) 96 hr after adding 15 nM a- thrombin or 30 μM TFLLRN-NH2, specific PAR1 agonist peptide, had not significantly increased the number. specific response of MKN45/PAR1 both to a-thrombin and TFLLR-NH2, demonstrating the presence of a func- tional receptor in these cells. PAR1 activation induces cell invasion MKN45/PAR1 stimulated either by a-thrombin or by TFLLR-NH2 showed significant acceleration of invasion (Figure 5), whereas invasion of MKN45/mock was not stimulated by either agonist (Figure 5). In regards to the proliferative response, the PAR1 antagonist SCH79797 inhibited invasion triggered by both PAR1 agonists (Fig- ure 5). This result further supports that the a-throm- bin-mediated responses in MKN45/PAR1 were due to PAR1 activation. Figure 3 Proliferation assay in MKN45/PAR1 with a-thrombin stimulation. MKN45/PAR1 (1.0×104 cells/well) 96 hr after adding 15 nM a- thrombin had significantly increased the number. SCH79797, selective PAR1 antagonist, significantly reversed the growth rate of MKN45/PAR1 at 35 and 70 nM and completely abolished thrombin dependent growth progression at 150 nM in the presence of 15 nM a-thrombin.