Fig. 6: Silencing MUC1-C inhibits MCC self-renewal capacity and tumorigenicity.

A Representative images of tumorspheres derived from WaGa/tet-MUC1shRNA cells treated with control vehicle or DOX for 7 days (left). Bar represents 50 microns. The number of tumorspheres is expressed as the mean ± SD of three determinations (right). B, C Six-week-old NSG mice were injected subcutaneously in the flank with 1 × 10⁷ WaGa/tet-MUC1shRNA cells. Mice were pair-matched into two groups when tumors reached 100–150 mm³ and were fed without and with DOX. Tumor volumes are expressed as the mean ± SEM for six mice (B). Lysates from untreated and DOX-treated WaGa/tet-MUC1shRNA tumors obtained on day 5 were immunoblotted with antibodies against the indicated proteins (C). D Representative images of tumorspheres derived from MKL-1/tet-MUC1shRNA cells treated with control vehicle or DOX for 7 days (left). Bar represents 50 microns. The number of tumorspheres is expressed as the mean ± SD of three determinations (right). E, F. Six-week-old NSG mice were injected subcutaneously in the flank with 1 × 10⁷ MKL-1/tet-MUC1shRNA cells. Mice were pair-matched into two groups when tumors reached 100–150 mm³ and were fed without and with DOX. Tumor volumes are expressed as the mean ± SEM for six mice (E). Lysates from untreated and DOX-treated MKL-1/tet-MUC1shRNA tumors obtained on day 7 were immunoblotted with antibodies against the indicated proteins (F). G Representative images of tumorspheres derived from MCC26/tet-MUC1shRNA cells treated with control vehicle or DOX for 7 days (left). Bar represents 50 microns. The number of tumorspheres is expressed as the mean ± SD of three determinations (right).