Abstract
An Ha-ras oncogene was isolated from a cell line of gastric carcinoma called BGE-823 in order to elucidate genetic control and the influence of DNA sequences. The oncogene was cloned and identified as a single nucleotide substitution of thymine for guanine in the 12th codon through the sequencing of its first axon. We compared the differences of expression and regulation between the transformed Ha-ras cells and untransformed parent cells. Data indicated that the expression of Ha-ras in the transformed cells was five-fold higher than in the untransformed cells and that the Ha-ras gene in the former was hypersensitive toward DNase I. In addition, a nuclear protein of 35 kilodaltons bound strongly to the 2.5 Kb fragment located upstream of the 6.6 Kb Ha-ras gene and contained a GC rich region. These results suggest that there might be another mechanism of activation for the ras gene besides point mutation.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Franza B Jr, et al. In vitro establishment is not a sufficient prerequisite for transformation by activated ras oncogenes. Cell 1986; 44:409.
Damamte G, et al. Nucleotide sequence and characterization of the 5′ flanking region of the rat Ha-ras protooncogene. PNAS, USA 1987; 84:774.
Wasylyk C, et al. The c-Ha-ras oncogene and a tumor promoter activate the polyoma virus enhancer. Cell 1987; 48:525.
Deng Guoren, et al. Activated c-Ha-ras oncogene with a guanine to thymine transvertion at the twelfth codon in a human stomach cancer cell line. Cancer Res 1987; 47:3195.
宋 建国, 等. 简化的质粒 PEJ 6.6 DNA 制 备方法. 癌症 1987.5 370
Maniatis T, et al. Molecular cloning: A laboratory manual, Cold Spring Harbor Laobratory 1982.
Adrian GS, et al. Adenosine deaminase messenge RNAs in lymphoblast cell lines derived from leukemia patients with hereditary adenosine deaminase deficiency. J Clin Invest 1983; 71:1649.
Lawson GM, et al. Deoxyribonuclease I sensitivity of the nontranscribed sequences flanking the 5′ and 3′ ends of the ovomucoid gene and the ovalbumin and its related X and Y genes in hen oviduct nuclei. Biochemistry 1980; 19:4403.
Siebenlist U, et al. Chromatin structure and protein binding in the putative regulatory region of the c-myc gene in Burkitt lymphoma. Cell 1984; 37:381.
Kvesdi I, et al. Identification of a cellular transcription factor involved in E1A trans-activation. Cell 1986; 45:219.
Sassone-Carsi P, et al. Modulation of c-fos gene transcription by negative and positive cellular factors. Nature 1987; 326(6112):507.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Han, F., Liu, S., Song, J. et al. Differences in expression and regulation between transformed cells of the human gastric carcinoma oncogene Ha-ras and the untransformed parent cells. Chinese Journal of Cancer Research 1, 17–22 (1989). https://doi.org/10.1007/BF02683531
Issue Date:
DOI: https://doi.org/10.1007/BF02683531