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Comparative Transfer RNA Methylase Capacity in Mouse Ascites Tumors and in Their Derived Tumorigenic and Nontumorigenic Cell Cultures¹

Department of Cancer Research, University of Saskatchewan, Saskatoon, Saskatchewan, Canada

The transfer RNA (tRNA) methylase activity from two types of mouse ascites tumor cells (TA3 adenocarcinoma and 6C3HED lymphosarcoma) was compared to that of derived tumorigenic and nontumorigenic cultured cells of the same cell types. The nontumorigenic cells had lost their ability to produce tumors on back transplantation by extended passage in cell culture. The two ascites cell types differed in their capacity to methylate Escherichia coli B tRNA. The TA3 cells had an approximately 30% greater capacity than did the 6C3HED cells. There was no difference in the methylating capacity of either cell line during in vivo tumor development. Cell extracts from 9-day TA3 ascites tumors and from TA3 tumorigenic cultured cells exhibited between 50 and 60% more methylating ability than did extracts from nontumorigenic cultured cells of the same cell line. Contrary to this, 9-day 6C3HED ascites cell extracts showed no difference in tRNA methylase activity when compared to extracts from 6C3HED nontumorigenic cultured cells. These results indicate that a quantitative alteration in tRNA methylase activity may not necessarily be associated with loss of tumorigenicity in this ascites cell system.

In a control experiment, it was found that the tRNA methylase activity of a solid, s.c., 3-methylcholanthrene-induced transplantable mouse tumor was 35% greater than that of normal mouse liver or kidney and 80% greater than that of normal mouse lung. This observation is in accord with previous reports by other authors that tRNA methylase activity of some neoplastic tissues and cells is increased in comparison with normal tissue.

¹ Supported by the National Cancer Institute of Canada.

² Present address: The Samuel Roberts Noble Foundation, Inc., P. O. Box 878, Ardmore, Okla. 73401.

³ Research Associate of the National Cancer Institute of Canada and the person to whom requests for reprints should be addressed.

⁴ Present address: Department of Biochemistry, University of Saskatchewan, Saskatoon, Canada.

Received 9/21/70. Accepted 1/15/71.