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首页> 外文期刊>Cell biology international. >SV-40 large T antigen reversibly inhibits expression of tyrosinase, TRP-1, TRP-2 and Mitf, but not Pax-3, in conditionally immortalized mouse melanocytes.
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SV-40 large T antigen reversibly inhibits expression of tyrosinase, TRP-1, TRP-2 and Mitf, but not Pax-3, in conditionally immortalized mouse melanocytes.

机译：SV-40大T抗原可逆地抑制条件永生的小鼠黑素细胞中酪氨酸酶，TRP-1，TRP-2和Mitf的表达，但不抑制Pax-3的表达。

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摘要

Transformation of mouse melanocytes with a variety of exogenous oncogenes or chemical carcinogens frequently results in irreversible loss of pigmentation. We have infected mouse melanocytes with a temperature-sensitive mutant of the simian virus 40 (SV40) large tumour antigen to study the molecular mechanisms underlying depigmentation during melanocyte transformation. The results show that, out of six cell lines analyzed at the permissive temperature of the oncoprotein, three epidermal and two dermal melanocyte clones remained pigmented and retained the ability to synthesize melanin and to express the melanocyte-specific genes, including tyrosinase, tyrosinase related protein-1, tyrosinase related protein-2 and Mitf. In contrast, one dermal melanocyte clone (DMEL-3) gradually depigmented. This depigmentation was characterized by enhanced growth and down-regulation of melanocyte-specific gene expression. When the oncogene was inactivated by culture at the non-permissive temperature, the pigmented phenotype in DMEL-3 cells could be rescued, and there was a corresponding time-dependent increase in melanocyte-specific gene expression. After extended passage, this rescue could not be achieved. Our results provide direct evidence for the role of the SV40 large T antigen in melanocyte de-differentiation. Expression of Pax-3, a transcription factor implicated in melanocyte differentiation, was unaltered during the SV40-initiated de-differentiation, and de-differentiated melanocytes expressed normal levels of Pax-3 message. We speculate on the mechanism by which the oncoprotein might be regulating Mitf gene expression and of the role of Pax-3 in this process. Copyright 2001 Academic Press.
机译：具有多种外源性致癌基因或化学致癌物的小鼠黑素细胞的转化常常导致不可逆的色素沉着损失。我们用猿猴病毒40（SV40）大肿瘤抗原的温度敏感突变体感染了小鼠黑素细胞，以研究黑素细胞转化过程中色素沉着的分子机制。结果表明，在癌蛋白的允许温度下分析的六种细胞系中，三个表皮和两个真皮黑素细胞克隆保持色素沉着，并具有合成黑素和表达黑素细胞特异性基因（包括酪氨酸酶，酪氨酸酶相关蛋白）的能力。 -1，酪氨酸酶相关蛋白2和Mitf。相反，一个真皮黑素细胞克隆（DMEL-3）逐渐脱色。这种色素沉着的特征在于黑色素细胞特异性基因表达的增强生长和下调。当在非允许温度下通过培养使癌基因失活时，可以挽救DMEL-3细胞中的色素表型，并且黑素细胞特异性基因表达也随时间增加。长时间通过后，无法实现这种救援。我们的结果为SV40大T抗原在黑素细胞去分化中的作用提供了直接的证据。在SV40引发的去分化过程中，Pax-3（一种涉及黑色素细胞分化的转录因子）的表达未改变，并且去分化的黑色素细胞表达了正常水平的Pax-3信息。我们推测癌蛋白可能调控Mitf基因表达的机制以及Pax-3在此过程中的作用。版权所有2001，学术出版社。

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