Figure 4
From: Acquisition of a side population fraction augments malignant phenotype in ovarian cancer
Target genes regulate tumor initiating ability and in vivo tumor proliferation, and suppression of six genes enhances resistance to chemotherapeutic agents. (a,b) Newly generated SP cells exhibit greater tumor initiating capability than do MP cells and control cells. Data from CH1-control, SP and MP cells derived from CH1 sh-target gene cells are shown. Num; Number, cont; control-MP. (a) Limiting dilution assay results. (b) Tumor growth curves generated from injection of 1 × 103 indicated cells. (c,d) Newly generated SP cells exhibit greater tumor initiating capability than do MP cells and control cells. Data showing tumor initiating ability for SKOV3-control, SP and MP derived from SKOV3 sh-target gene cells are shown. Num; Number, cont; control-MP. (c) Limiting dilution assays. (d) Tumor growth curves generated from injection of 1 × 102 indicated cells. (e–g) Overexpression of VPS45, TLE2, ZNF498 decreases in vivo tumor proliferation. (e) Tumor growth curves generated from injection of 1 × 105 A2780 control or ORF-VPS45 cells. (f) Tumor growth curves generated from injection of 1 × 105 A2780 control or ORF-TLE2 cells. (g) Tumor growth curves generated from injection of 1 × 106 IGROV1 control or ORF-ZNF498 cells. (h,i) Suppression of six genes enhances resistance to chemotherapeutic agents. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. (h) IC50 values for CH1-control, sh-MSL3, sh-ZNF691 and sh-VPS45 cells treated with Cisplatin (CDDP), Gemcitabine (GEM), doxorubicin (Doxil) and paclitaxel (PTX). (i) IC50 values for SKOV3-control, sh-ITGB3BP, sh-TLE2 and sh-ZNF498 cells treated with CDDP, Gemcitabine (GEM), doxorubicin (Doxil) and paclitaxel (PTX).
