Fig. 6
From: AIM1 is an actin-binding protein that suppresses cell migration and micrometastatic dissemination
AIM1 depletion results in increased micrometastatic dissemination in vivo. Xenograft tumors derived from sh-control and sh-AIM1 expressing PC3 and VCaP prostate cancer cell lines (five animals per group) were grown in the flank of nude mice for 4 and 6 weeks, respectively. a, c Tumor weights at the time of necropsy of PC3 and VCaP xenografts. Note that there was no statistically significant difference in end of study tumor weights between sh-control and sh-AIM1 xenografts of PC3 and VCaP cells. b, d Cell proliferation as determined by Ki67 immunostaining is not different in sh-control and sh-AIM1 xenografts. The percentage of Ki67 positive cells is indicated. Scale bars indicate 50 μm. e Representative micrographs of immunostains for AIM1 and actin in PC3 sh-control and sh-AIM1 xenograft tumors demonstrate significant depletion of AIM1 protein levels in sh-AIM1 tumors and increased cytoplasmic staining of actin. Scale bars indicate 50 μm. f Micrometastatic burden, measured as PC3 cell equivalents, as determined by Alu-specific quantitative PCR in liver, lung and spleen from sh-control and sh-AIM1 PC3 xenograft bearing animals (n = 5 in each group). g Representative micrographs of immunostains for AIM1 and actin in VCaP sh-control and sh-AIM1 xenograft tumors demonstrate significant depletion of AIM1 protein levels in sh-AIM1 tumors and increased cytoplasmic staining of actin. h Micrometastatic burden, measured as VCaP cell equivalents, as determined by Alu-specific quantitative PCR in liver, lung and spleen from sh-control and sh-AIM1 bearing animals (n = 5 in each group). *P < 0.05, **P < 0.01 (t-test P values)
