We have previously shown by examining the anchorage dependence, density-dependent inhibition of growth, LETS protein and microfilament bundles that the transformed phenotype of the parental tumours are suppressed in hybrids between rat embryo fibroblast (REF) and mouse tumour cells (TA3B). Hybrids between TA3B and Syrian hamster sarcoma cells (BHK-B1) also show suppression. We now demonstrate that tumorigenicity in nude mice is also suppressed in TA3B X REF and B1 X TA3B hybrids. Tumours arise from the suppressed hybrids by the selective outgrowth of variants with properties different from the majority of cells inoculated. These tumour variants always had an altered cytoskeletin but 1 out of 14 cases retained anchorage-dependent growth. Selection in culture for anchorage-independent growth selected for tumorigenicity. The coordinate suppression of the transformed phenotype and tumorigenicity could be explained by postulating a pleiotropic control mechanism affecting both. However, the occasional dissociation of tumorigenicity from anchorage dependence in the variants suggests that the targets for the control mechanism must be different.
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JOURNAL ARTICLE| 01 October 1979
Expression of the transformed phenotype and tumorigenicity in somatic cell hybrids
Online Issn: 1477-9137
Print Issn: 0021-9533
© 1979 by Company of Biologists
J Cell Sci (1979) 39 (1): 319–327.
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C.J. Marshall; Expression of the transformed phenotype and tumorigenicity in somatic cell hybrids. J Cell Sci 1 October 1979; 39 (1): 319–327. doi: https://doi.org/10.1242/jcs.39.1.319
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