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Enzootic nasal tumor virus type 2 envelope of goats acts as a retroviral oncogene in cell transformation
Virus Genes ( IF 1.6 ) Pub Date : 2020-11-05 , DOI: 10.1007/s11262-020-01808-7
Naoyoshi Maeda 1 , Yasuo Inoshima 2 , Marcelo De Las Heras 3 , Katsumi Maenaka 1, 4
Affiliation  

Enzootic nasal tumor virus type 1 (ENTV-1) (ovine nasal tumor virus) and ENTV-2 (caprine nasal tumor virus) are known to be causative agents of enzootic nasal adenocarcinoma (ENA) in sheep and goats, respectively. Although the nucleotide and amino acid sequences of ENTV-1 and ENTV-2 are quite similar, they are recognized as phylogenetically distinct viruses. The envelope protein of ENTV-1 functions as an oncoprotein in the in vitro transformation of epithelial cells and fibroblasts. Thus, it is the primary determinant of in vivo tumorigenesis in ENA. As per our knowledge, no previous studies have reported in detail the role of ENTV-2 in ENA tumorigenesis. Here, in order to investigate the molecular mechanism of caprine ENA oncogenesis by ENTV-2, we have attempted to identify the transforming potential of ENTV-2 envelope, and investigated the activation of cell signaling pathways in oncogenic transformation. Our findings confirmed that ENTV-2 envelope was capable of inducing oncogenic transformation of rat cell lines in vitro. Further, we found that MAPK, Akt, and p38 were constitutively activated in ENTV-2 envelope-transformed clone cells. In addition, inhibitor experiments revealed that MEK-MAPK and PI3K-Akt signaling pathways are involved in the ENTV-2 envelope-induced cell transformation. These data indicate that ENTV-2 envelope could induce oncogenic transformation by signaling pathways that are also utilized by ENTV-1 envelope.



中文翻译:

山羊地方性鼻肿瘤病毒2型包膜在细胞转化中作为逆转录病毒致癌基因

已知地方性鼻肿瘤病毒 1 型 (ENTV-1)(绵羊鼻肿瘤病毒)和 ENTV-2(山羊鼻肿瘤病毒)分别是绵羊和山羊的地方性鼻腺癌 (ENA) 的病原体。尽管 ENTV-1 和 ENTV-2 的核苷酸和氨基酸序列非常相似,但它们被认为是系统发育不同的病毒。ENTV-1 的包膜蛋白在上皮细胞和成纤维细胞的体外转化中起癌蛋白的作用。因此,它是 ENA 体内肿瘤发生的主要决定因素。据我们所知,以前没有研究详细报道过 ENTV-2 在 ENA 肿瘤发生中的作用。在这里,为了研究 ENTV-2 对山羊 ENA 致癌的分子机制,我们试图确定 ENTV-2 包膜的转化潜力,并研究了致癌转化中细胞信号通路的激活。我们的研究结果证实,ENTV-2 包膜能够在体外诱导大鼠细胞系的致癌转化。此外,我们发现 MAPK、Akt 和 p38 在 ENTV-2 包膜转化的克隆细胞中被组成型激活。此外,抑制剂实验表明 MEK-MAPK 和 PI3K-Akt 信号通路参与了ENTV-2 包膜诱导的细胞转化。这些数据表明,ENTV-2 包膜可以通过也被 ENTV-1 包膜利用的信号通路诱导致癌转化。在ENTV-2包膜转化的克隆细胞中,p38和p38被组成型激活。此外,抑制剂实验表明 MEK-MAPK 和 PI3K-Akt 信号通路参与了ENTV-2 包膜诱导的细胞转化。这些数据表明,ENTV-2 包膜可以通过也被 ENTV-1 包膜利用的信号通路诱导致癌转化。在ENTV-2包膜转化的克隆细胞中,p38和p38被组成型激活。此外,抑制剂实验表明 MEK-MAPK 和 PI3K-Akt 信号通路参与了ENTV-2 包膜诱导的细胞转化。这些数据表明,ENTV-2 包膜可以通过也被 ENTV-1 包膜利用的信号通路诱导致癌转化。

更新日期:2020-11-06
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