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. 2020 May 8;11:2300. doi: 10.1038/s41467-020-16123-w

Fig. 8. RasV12-driven tumourigenesis depends on the setting of an IGF/InR autocrine activation loop.

Fig. 8

a, b Phosphorylation of 4E-BP, a downstream target of the PI3//AKT/mTOR pathway, is not detected in RasV12, EGFR RNAi expressing clones. c, d Phosphorylation of 4E-BP is detected in tumours induced by clonal expression of a constitutively active form of EGFR (EGFRl). e qPCR quantification reveals that IGF/Ilp6 (Ilp6) is overexpressed in glands displaying GFP-RasV12 expressing clones compared to control gland (left column, Two tailed Mann–Whitney test: P = 0,0079. RasV12-dependent overexpression of IGF/Ilp6 is suppressed by downregulation of ERK (ERK RNAi, right column, Two tailed Mann–Whitney test: P = 0,68). (f) qPCR quantification reveals that IGF/Ilp6 (Ilp6) is overexpressed in glands displaying GFP-EGFRl expressing clones compared to control gland (left column, Two tailed Mann–Whitney test: P = 0,0079. EGFRl-dependent overexpression of IGF/Ilp6 is suppressed by downregulation of Ras (Ras RNAi, right column, Two tailed Mann–Whitney test: P = 0,21). g Invasive tumour frequency of GFP-RasV12 expressing clones (RasV12) is impaired by downregulation of IGF/Ilp6 (Ilp6 RNAi) (Chi2 test; P < 0.0001). h Invasive tumour frequency of GFP-RasV12 expressing clones (RasV12) is impaired by co-expression of a dominant-negative form of InR (InR dn) (Chi2 test; P < 0.0001). Data are represented as mean values ± SEM. Representative images in (a–d) from three or more experiments. **P < 0.01; ****P < 0.0001. Scale bars: 50 μm.