| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1988: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1987: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
The mouse cell line MO-5 is resistant to transformation by various chemical carcinogens and also by UV irradiation (C. Yasutake, Y.Kuratomi, M.Ono, S.Masumi, and M.Kuwano, Cancer Res. 47: 4894-4899, 1987). Northern (RNA) blot analysis showed active expression of ras and myc genes in MO-5 and BALB/3T3 cells. The effect of transfection of various oncogenes on transformation was compared in MO-5 cells and parental BALB/3t3 cells. Activated c-H-ras, c-N-ras, and v-mos gene induced transformation foci of MO-5 and BALB/3t3. Introduction of the polyomavirus middle T-antigen (mTag) or the Rous sarcoma virus-related oncogene V-src, however, efficiently transformed BALB/3t3 but not MO-5 cells. Expression and phosphory-lation of mTag and the associated c-src proteins were observed in mTag-transfected clones of MO-5 as in BALB/3t3 and phosphorylation of the src protein was observed in v-src-trans-fected BALB/3T3 and MO-5 clone. Hybrids between mtag- or v-src-induced transformants of BALB/3T3 and untransforme MO-5 maintained the transformation phenotype, suggesting that no dominant suppressor of transformation exists in MO-5. A hybrid clone between BALB/3T3 and MO-5 induced effecient transformation foci after transfection with the mTag gene, suggesting that the deficient transformation phenotype of MO-5 was recessive. Instead, some other alteration of MO-5, plausibly membrane function, might lead to abortive trans-formation by chemical carcinogens and also by mTag and the v-src gene product.
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