作者: R. Plattner , M. J. Anderson , K. Y. Sato , C. L. Fasching , C. J. Der
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摘要: Abstract ras oncogenes are mutated in at variety of human tumors, which suggests that they play an important role carcinogenesis. To determine whether continued oncogenic ras expression is necessary to maintain the malignant phenotype, we studied fibrosarcoma cell line, HT1080, contains one and wild-type N-ras allele. We isolated a variant this line no longer contained copy gene. Loss mutant resulted cells displayed less transformed phenotype characterized by flat morphology, decreased growth rate, organized actin stress fibers, loss anchorage-independent growth. The was restored following reintroduction N-ras. Although drastically affected vitro parameters, remained tumorigenic nude mice indicating not for maintenance phenotype. confirmed latter observation colon carcinoma lines have lost activated K-ras via targeted knockout