| First Author | Honjo Y | Year | 2007 |
| Journal | Cell Cycle | Volume | 6 |
| Issue | 11 | Pages | 1360-6 |
| PubMed ID | 17534148 | Mgi Jnum | J:156004 |
| Mgi Id | MGI:4418443 | Doi | 10.4161/cc.6.11.4268 |
| Citation | Honjo Y, et al. (2007) TGF-beta receptor I conditional knockout mice develop spontaneous squamous cell carcinoma. Cell Cycle 6(11):1360-6 |
| abstractText | We generated a mouse model with a conditional deletion of TGF-beta signaling in the neurons by crossing TGF-beta receptor I (TbetaRI) floxed mice with neurofilament-H (NF-H) Cre mice. 35% of F1 conditional knockout (COKO) mice developed spontaneous squamous cell carcinomas (SCCs) in periorbital and/or perianal regions. Transplantation of these tumors into athymic nude mice resulted in 62% tumorigenicity. To determine whether evasion of the immune response plays any role in this tumorigenesis, we analyzed the expression levels of receptors for interleukin-13 (mIL-13R), a key negative regulator of tumor immunosurveillance, and found that 33% of COKO tumors expressed the IL-13R alpha2 chain. Primary cultures of the SCCs expressing IL-13R alpha2 were sensitive to the cytotoxic effect of IL-13R-directed cytotoxin treatment. This is the first demonstration that loss of TbetaRI can lead to spontaneous tumor formation. These mice can serve as a unique mouse model of SCC to evaluate the tumorigenicity and effect of anti-cancer therapeutics. |
