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

A variant clone resistant to high doses of colchicine (KB‐C1) derived from human cancer KB cell line is resistant to various anticancer agents. The KB‐C1 cells were much more resistant to epidermal growth factor and a chimeric toxin, EGF‐Pseudomottas exotoxin (PE), than the parental KB cells. KB‐C1 cells have decreased numbers of EGF‐receptors, though the affinity of the receptors is similar to that in the parental KB cells. A drug‐sensitive revertant (C1‐R2) partially recovered its EGF‐receptor activity. Northern blot analysis showed a decreased level of EGF‐receptor mRNA in KB‐C1 cells, while the multidrug‐resistance gene, mdr‐1, was expressed at very high levels in KB‐C1 cells, but not in KB or C1‐R2 cells. The drug‐resistant cells were less tumorigenic than the parental cells when injected into nude mice. A decreased expression of EGF‐receptor in these cells may be one of the pleiotropic properties of multidrug‐resistant cells and may perhaps represent the basis for their reduced tumorigenicity.

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 phosphorylation 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-transfected BALB/3T3 and MO-5 clones. Hybrids between mTag- or v-src-induced transformants of BALB/3T3 and untransformed 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 efficient 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 transformation by chemical carcinogens and also by mTag and the v-src gene product.