Expression of tyrosinase-related protein 2/DOPAchrome tautomerase in the retinoblastoma.
Expression of tyrosinase-related protein 2/DOPAchrome tautomerase in the retinoblastoma.
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酪氨酸酶相关蛋白2/DOPAchrome互变异构酶在视网膜母细胞瘤中的表达。
DOI：
10.1006/exer.2000.0948
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发表时间：
2001
影响因子：
3.4
通讯作者：
S. Shibahara
中科院分区：
文献类型：
--
作者：
T. Udono;K. Takahashi;K. Yasumoto;M. Yoshizawa;K. Takeda;T. Abe;M. Tamai;S. Shibahara
酪氨酸酶相关蛋白2(TRP-2)，又称DOPA铬互变异构酶，是黑色素生物合成过程中的一种酶，在DOPA代谢产物的解毒过程中起着重要作用。Trp-2在神经沟来源的黑素细胞和视杯来源的视网膜色素上皮(RPE)中表达。Trp-2已被确定为黑素母细胞和RPE的早期分化标志物。因此，研究Trp-2/DOPAChrome互变异构酶的表达调控具有重要意义。在这里，我们发现TRP-2mRNA在Y79人视网膜母细胞瘤细胞系中表达，该细胞系来源于原始的多潜能视网膜细胞。视网膜母细胞瘤是儿童常见的原发眼内肿瘤。在Y79视网膜母细胞瘤细胞中，Trp-2mRNA和蛋白的基础表达水平与黑色素瘤细胞相当，而在视网膜母细胞瘤细胞中检测不到酪氨酸酶的mRNA，酪氨酸酶是黑素合成的限速酶。瞬时转染实验表明，Trp-2基因启动子能有效地引导报告基因在视网膜母细胞瘤细胞中的表达，就像在黑色素瘤细胞中一样。此外，视黄酸可诱导视网膜母细胞瘤细胞TRP-2mRNA的表达，而cAMP升高剂Forsklin对其影响不明显，而在黑色素瘤细胞中，Forsklin可诱导其表达，但维甲酸不能诱导其表达。这些结果表明，视网膜母细胞瘤和黑色素瘤细胞对Trp-2表达的调控存在差异。此外，RT-PCR检测，视网膜母细胞瘤切除标本中有Trp-2mRNA的表达。本研究显示了Trp-2的意外特征，并可能增强我们对视网膜母细胞瘤的病理生理学的理解。
Tyrosinase-related protein 2 (TRP-2), also known as DOPAchrome tautomerase, is an enzyme in melanin biosynthesis and may play an important role in detoxification of a metabolite derived from DOPA. TRP-2 is expressed in melanocytes of neural crest origin and retinal pigment epithelium (RPE), derived from the optic cup. TRP-2 has been established as an early differentiation marker for melanoblasts and RPE. It is therefore of significance to study the regulation of TRP-2/DOPAchrome tautomerase expression. Here we show that TRP-2 mRNA is expressed in Y79 human retinoblastoma cell line, derived from a primitive multipotential retinal cell. Retinoblastoma is the common primary intraocular tumor of childhood. Basal expression levels in Y79 retinoblastoma cells of TRP-2 mRNA and protein are comparable to those in melanoma cells, whereas mRNA for tyrosinase, the rate-limiting enzyme in melanogenesis, is undetectable in retinoblastoma cells. Transient transfection assays showed that the TRP-2 gene promoter efficiently directs the reporter gene expression in retinoblastoma cells as it does in melanoma cells. Moreover, the expression of TRP-2 mRNA was induced by retinoic acid in retinoblastoma cells but not noticeably affected by forskolin, a cAMP-elevating reagent, whereas in melanoma cells its expression was induced by forskolin but not by retinoic acid. These results suggest a difference in the regulation of TRP-2 expression between retinoblastoma and melanoma cells. Moreover, TRP-2 mRNA is expressed in the excised retinoblastoma specimens, as assessed by RT-PCR. The present study shows unexpected features of TRP-2 and may enhance our understanding of the pathophysiology of retinoblastoma.
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DOI：
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发表时间：
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