Rat 3Y1 Cell Retains Suppressive Activity for HTLV-I TAX-mediatedTransformation

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Tax is an own transcriptional activator of human T-cell leukemia virus type I (HTLV-I) virus which is a causative agent of adult T-cell leukemia (ATL). Expression of the Tax protein in the rodent fibrolast, Rat-l cells, leads to an anchorage independent growth in soft agar and tumor formation in athymic mice. Rat 3Y1 cells, originating from Fisher Rat fibroblasts, are known to be a permanent cell line exhibiting a normal phenotype and have been used for assays of transformation by several oncogenes. Although Tax was able to trans-activate satisfactorily the HTLV-I long terminal repeat (LTR) and NF-κB dependent promoter in 3Y1 cells, the cells expressing Tax could neither form visible colonies in soft agar nor elicit tumors in nude mice. Cell fusion experiments suggested that 3Y1 cells might have some dominant suppressive activities for Tax-mediated transformation. Since the constitutive activation of the NF-κB pathway is suggested to be responsible for Tax-mediated transformation of rat fibroblasts, 3Y1 cells might be useful materials to obtain suppressor candidates related to the NF-κB family involved in oncogenic properties or to elucidate other unknown pathways for Tax-mediated transformation of the rat fibroblast. At least p53 mutation is not involved in cooperation with interaction of tax gene for transformation.
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