Fig. 1.

Tumor growth in Tspan8ko- and/or CD151ko-mice. Wt and ko mice received a sc injection of 2 × 10⁶ wt- or ko-MCA cells. a Initiation of tumor growth and mean tumor diameter (6 mice/group); b survival and mean survival time of wt- and ko-mice after sc injection of wt- and ko-MCA tumor cells (5 mice/group); p-values are indicated; c No of mice with migrating tumor cells (PB) and micrometastases in draining LN, BM, lung and liver and mean frequency of mice with disseminated tumor cells per tumor, per mice and per organ; p-values (after Bonferroni Holm correction) are indicated; d Tabular overview of shock frozen tumor sections (immunohistochemistry) of tetraspanins, adhesion molecules, proteases and angiogenesis-related factors / receptors in wt- and ko-MCA tumors grown in wt and ko mice. Expression was judged as +++: very strong, ++: strong, +: distinct, ±: weak, ±: very weak; e immunohistochemistry examples of tetraspanin expression in wt and ko MCA grown in wt and ko mice (scale bar: 100 μm). Tumor growth initiation of wt- and ko-MCA tumors is retarded in ko mice and tumor growth progresses very slowly. Tumor cell dissemination is severely impaired in ko mice, but ko MCA dissemination is promoted in wt mice accompanied by upregulation of adhesion molecules, proteases and angiogenesis markers. Dbko-MCA cells grown in dbko mice were very necrotic. The findings indicate compensatory activities of the host