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. 2013 Jul 14;4(8):1212–1229. doi: 10.18632/oncotarget.1130

Figure 7. Effect of a SMIP004 analog on tumor growth in vivo.

Figure 7

(A) The chemical structures of parent compound SMIP004 and its analog SMIP004-7 are shown in the top panel. The middle panel shows the effect of several SMIP004 analogs on UPR activation and cell cycle regulators. LNCaP-S14 cells were treated with DMSO (0.1%), SMIP004 (40 μM), SMIP004-7 (40 μM), or the inactive analogs P53802 (40 μM), AB132168 (40 μM) for 24 h. UPR activation and cell cycle regulators were analyzed by immunoblotting. The glycosylation inhibitor tunicamycin (TM, 1 μM) was used as a positive control for UPR induction. Cell viability was measured by MTT assay in cells treated with SMIP004 or SMIP004-7 (lower panel). The graph represents the mean of four replicates ± standard deviations. (B) LNCaP-S14 xenografts were grown in SCID mice. Six animals received SMIP004-7 (50 mg/kg i.p.) for 10 days while the remaining six mice were treated with vehicle. The graph represents mean tumor volumes ± standard deviations in each group over time. (C) Final weights of tumors excised from mice treated with vehicle or SMIP004-7. The graph represents the average of three mice ± standard deviations. (D) The response to SMIP004-7 or vehicle for individual animals was expressed as change in tumor volume (i.e. day 9 minus day 0). (E) The graph represents relative average body weights ± standard deviations in the SMIP00-7 treatment and DMSO control groups.