Figure 5
Figure 5. Inactivation of Rce1 inhibits the growth of K-RASG12D–expressing fibroblasts. (A) Cell proliferation assay of spontaneously immortalized Rce1fl/flKLSL and Rce1fl/+KLSL embryonic fibroblasts treated with Cre and β-gal-adenoviruses. Data are mean of 2 independent cell lines per genotype. The experiment was repeated with a pair of primary cell lines and yielded similar results. (B) PCR amplification of genomic DNA from the cells in panel A demonstrating the activation of the Kras2G12D allele and the inactivation of the Rce1fl allele. Lane 1, β-gal-adenovirus-treated Rce1fl/+KLSL cells; lane 2, Cre-adenovirus-treated Rce1fl/+KLSL cells; lane 3, β-gal-adenovirus–treated Rce1fl/flKLSL cells; lane 4, Cre-adenovirus-treated Rce1fl/flKLSL cells.

Inactivation of Rce1 inhibits the growth of K-RASG12D–expressing fibroblasts. (A) Cell proliferation assay of spontaneously immortalized Rce1fl/flKLSL and Rce1fl/+KLSL embryonic fibroblasts treated with Cre and β-gal-adenoviruses. Data are mean of 2 independent cell lines per genotype. The experiment was repeated with a pair of primary cell lines and yielded similar results. (B) PCR amplification of genomic DNA from the cells in panel A demonstrating the activation of the Kras2G12D allele and the inactivation of the Rce1fl allele. Lane 1, β-gal-adenovirus-treated Rce1fl/+KLSL cells; lane 2, Cre-adenovirus-treated Rce1fl/+KLSL cells; lane 3, β-gal-adenovirus–treated Rce1fl/flKLSL cells; lane 4, Cre-adenovirus-treated Rce1fl/flKLSL cells.

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