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首页> 外文期刊>Molecular and Cellular Biology >Interferon Regulatory Factor 4 Contributes to Transformation of v-Rel-Expressing Fibroblasts
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Interferon Regulatory Factor 4 Contributes to Transformation of v-Rel-Expressing Fibroblasts

机译：干扰素调节因子4有助于表达v-Rel的成纤维细胞的转化

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The avian homologue of the interferon regulatory factor 4 (IRF-4) and a novel splice variant lacking exon 6, IRF-4ΔE6, were isolated and characterized. Chicken IRF-4 is expressed in lymphoid organs, less in small intestine, and lungs. IRF-4ΔE6 mRNA, though less abundant than full-length IRF-4, was detected in lymphoid tissues, with the highest levels observed in thymic cells. IRF-4 is highly expressed in v-Rel-transformed lymphocytes, and the expression of IRF-4 is increased in v-Rel- and c-Rel-transformed fibroblasts relative to control cells. The expression of IRF-4 from retrovirus vectors morphologically transformed primary fibroblasts, increased their saturation density, proliferation, and life span, and promoted their growth in soft agar. IRF-4 and v-Rel cooperated synergistically to transform fibroblasts. The expression of IRF-4 antisense RNA eliminated formation of soft agar colonies by v-Rel and reduced the proliferation of v-Rel-transformed cells. v-Rel-transformed fibroblasts produced interferon 1 (IFN1), which inhibits fibroblast proliferation. Infection of fibroblasts with retroviruses expressing v-Rel resulted in an increase in the mRNA levels of IFN1, the IFN receptor, STAT1, JAK1, and 2′,5′-oligo(A) synthetase. The exogenous expression of IRF-4 in v-Rel-transformed fibroblasts decreased the production of IFN1 and suppressed the expression of several genes in the IFN transduction pathway. These results suggest that induction of IRF-4 expression by v-Rel likely facilitates transformation of fibroblasts by decreasing the induction of this antiproliferative pathway.
机译：分离并鉴定了干扰素调节因子4（IRF-4）的禽同源物和缺少外显子6，IRF-4ΔE6的新型剪接变体。鸡IRF-4在淋巴器官中表达，在小肠和肺中表达较少。 IRF-4ΔE6mRNA虽然不如全长IRF-4丰富，但在淋巴组织中检测到，在胸腺细胞中观察到最高水平。相对于对照细胞，IRF-4在v-Rel转化的淋巴细胞中高度表达，IRF-4的表达在v-Rel和c-Rel转化的成纤维细胞中增加。逆转录病毒载体中IRF-4的表达在形态上转化了原代成纤维细胞，增加了其饱和密度，增殖和寿命，并促进了它们在软琼脂中的生长。 IRF-4和v-Rel协同合作转化成纤维细胞。 IRF-4反义RNA的表达消除了v-Rel形成的软琼脂菌落，并减少了v-Rel转化细胞的增殖。 v-Rel转化的成纤维细胞产生干扰素1（IFN1），抑制成纤维细胞增殖。成纤维细胞被表达v-Rel的逆转录病毒感染导致IFN1，mRNA受体，STAT1，JAK1和2'，5'-oligo（A）合成酶的mRNA水平增加。 IRF-4在v-Rel转化的成纤维细胞中的外源表达降低了IFN1的产生，并抑制了IFN转导途径中几个基因的表达。这些结果表明通过v-Rel诱导IRF-4表达可能通过减少该抗增殖途径的诱导而促进成纤维细胞的转化。

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