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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Multiple cells-of-origin of mutant K-Ras–induced mouse lung adenocarcinoma
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Multiple cells-of-origin of mutant K-Ras–induced mouse lung adenocarcinoma

机译：Multiple cells-of-origin of mutant K-Ras–induced mouse lung adenocarcinoma

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Much controversy surrounds the cell-of-origin of mutant K-Ras (K-RasG12D)–induced lung adenocarcinoma. To shed light on this issue, we have used technology that enables us to conditionally target K-RasG12D expression in Surfactant Protein C (SPC)~+ alveolar type 2 cells and in Clara cell antigen 10 (CC10)~+ Clara cells by use of cell-type–restricted recombinant Adeno-Cre viruses. Experiments were performed both in the presence and absence of the tumor suppressor gene p53, enabling us to assess what effect the cell-oforigin and the introduced genetic lesions have on the phenotypic characteristics of the resulting adenocarcinomas. We conclude that both SPC-expressing alveolar type 2 cells and CC10-expressing Clara cells have the ability to initiate malignant transformation following the introduction of these genetic alterations. The lungs of K-Ras~(lox– Stop–lox–G12D/+) and K-Ras~(lox–Stop–lox–G12D/+);tumor suppressor gene Trp53~(F/F) mice infected with Adeno5–SPC–Cre and Adeno5– CC10–Cre viruses displayed differences in their tumor spectrum, indicating distinct cellular routes of tumor initiation. Moreover, using a multicolor Cre reporter line, we demonstrate that the resulting tumors arise from a clonal expansion of switched cells. Taken together, these results indicate that there are multiple cellular paths to K-RasG12D–induced adenocarcinoma and that the initiating cell influences the histopathological phenotype of the tumors that arise.

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