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Department of Microbiology and Cancer Research Center, Boston University School of Medicine, Boston, Massachusetts 02118
By continuous in vitro passage in lipid-depleted media of a Kirsten sarcoma virus-transformed murine cell line (FK3T3), a new cell line has been established (AK3T3) which exhibits many of the in vitro growth characteristics of the untransformed parent cell line, BALB/3T3, A31 strain. The tumorigenicity of the AK3T3 cell line was compared with FK3T3 cells in mice fed diets varying in levels of polyunsaturated fatty acids (PUFA). Tumorigenicity of FK3T3 cells increased as the PUFA level decreased. On the other hand, tumorigenicity of AK3T3 cells decreased as dietary PUFA levels decreased. Fatty acid composition and membrane microviscosities did not differ significantly between the two strains, although both differed from those of the BALB/3T3 parent strain. A correlation between tumorigenicity and cholesterol content was observed. The cholesterol levels of the FK3T3 strain were uninfluenced by medium cholesterol levels, whereas the AK3T3 and the parent BALB/3T3 cells were markedly altered, such that both strains had low levels when grown in delipidized media. Thus, when grown in vivo in mice fed a diet very low in PUFA and cholesterol, AK3T3 cells had lowered tumorigenicity, whereas FK3T3 cells which can maintain their cholesterol levels under these conditions were quite tumorigenic. AK3T3 cells were less able than FK3T3 cells to produce an immune response in vivo and to respond to specific cell-mediated cytolysis. It was suggested that the use of these mostly isogenic tumor strains may offer a good model system to elucidate the specific cellular alteration which affects the responses of different tumors to dietary PUFA.
1 This work was supported by Grant PDT-82 from the American Cancer Society, a grant from Hoffmann LaRoche, Inc., and the National Large Bowel Cancer Project of National Cancer Institute, NIH CA 16750.
2 To whom requests for reprints should be addressed.
Received 11/27/78. Accepted 7/24/79.
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