Fig. 7

The activation of tumorigenic pathways by overexpressing oncogenic KRAS and mutant TP53 in the imPAC2 cells. Retroviral vectors expressing oncogenic human KRAS and mutant TP53-R273H were stably transduced into imPAC2 cells, resulting in the imPAC2-KRAS/TP53R273H cell line. The expression of KRAS and TP53R273H was confirmed by qPCR (Additional file 1: Figure S2B). Subconfluent imPAC2 and imPAC2-KRAS/TP53R273H cells were harvested, resuspended in PBS alone or PPCNg/PBS and subcutaneously injected into the flanks of athymic nude mice. At 30 days after injection, in the absence of PPCNg scaffold subcutaneous masses were only found in the imPAC2-KRAS/TP53R273H injection group, but not in the imPAC2 group (A-a), followed by H & E histologic analysis (A-b). Subcutaneous masses were retrieved from both imPAC2-KRAS/TP53R273H injection group and the imPAC2 group, and subjected to H & E staining (B-ab). Representative results are shown. Total RNA was also isolated from the retrieved masses in the PPCNg groups and subjected to qPCR analysis of the expression of RAS-MAK pathway genes (C-a), PI3K/AKT/mTOR pathway genes (C-b), and lung cancer-associated genes (C–c). Gapdh was used as the reference gene. “**” p < 0.01, “*” p < 0.05, compared with that of the imPAC2 control group