Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation.

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作者：

J Campisi，HE Gray，AB Pardee，M Dean，GE Sonenshein

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摘要：

Cellular oncogenes are DNA sequences implicated in the genesis of cancer, but their functions in the transformation process are not understood. Our experiments provide data linking expression of two well-studied proto-oncogenes, c- myc and c- ras Ki, to current knowledge of proliferation control and its perturbation by differentiation and chemical transformation. Growth stimulation of quiescent cells by serum elevates expression of the myc proto-oncogene in Balb/c 3T3 (A31) cells. In two chemically transformed A31 derivatives (BPA31 and DA31), c- myc expression is constitutive. The levels of c- myc mRNA in quiescent and growing transformed cells are nearly the same, and are only slightly elevated compared to the level found in growing A31 cells. By contrast, c- ras Ki expression is cell-cycle-dependent in BPA31 cells. The relative abundance of c- ras Ki mRNA begins to increase in mid- to late G0/G1. During terminal differentiation of teratocarcinoma stem cells (F9) into nonproliferating endoderm, relative mRNA abundance is diminished more markedly for c- myc than for c- ras Ki. These results demonstrate that expression of the myc and ras Ki protooncogenes is dependent upon the cellular growth state, and that growth control exhibits growth-factor-dependent, cell-cycle-timed oncogene expression. In the case of the BPA31 cells, c- myc is not rearranged, amplified, or overexpressed. However, the oncogene has lost its cycle-dependent regulation in the chemically transformed cells.

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关键词：

Animals Mice, Inbred BALB C Mice Cell Line Cell Transformation, Neoplastic Histones Kinetics Oncogenes Cell Division Cell Differentiation