Canine Papillomavirus 2 E6 Does Not Interfere With UVB-Induced Upregulation of p53 and p53-Regulated Genes.
Canine Papillomavirus 2 E6 Does Not Interfere With UVB-Induced Upregulation of p53 and p53-Regulated Genes.
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犬乳头瘤病毒2型E6不干扰UVB诱导的p53和p53调节基因的上调。
DOI：
10.3389/fvets.2021.570982
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发表时间：
2021
影响因子：
3.2
通讯作者：
Luff J
中科院分区：
文献类型：
--
作者：
Quinlan S;May S;Weeks R;Yuan H;Luff J
皮肤乳头瘤病毒是一种致癌病毒，可引起严重、持续的感染，这些感染可在免疫缺陷个体（例如X连锁严重联合免疫缺陷（XSCID）患者）暴露于紫外线（UV）的皮肤内发展为皮肤癌。XSCID的犬研究模型表现出类似的表型;这些犬发生严重的犬乳头瘤病毒2（CPV 2）感染，通常进展为癌症。因此，狗是一个自然的，自发的模型，研究皮肤乳头瘤病毒感染的免疫缺陷患者。人乳头瘤病毒癌基因E6部分通过启动肿瘤抑制蛋白p53的降解或通过抑制细胞生长停滞和凋亡途径内所需的p53依赖性基因的上调，从而导致肿瘤发生所需的DNA损伤的积累，从而促进癌症的发展。目前，人们对CPV 2及其如何促进癌症发展知之甚少。本研究的目的是确定是否CPV 2癌基因E6同样影响p53激活后，由紫外线辐射，以及下游p53调控基因控制生长停滞和凋亡。我们确定，皮肤CPV 2 E6不降解p53，或干扰p53调节基因p21，Bax，巴克，或lncRNA-p21的上调，这表明，CPV 2可能使用一个p53非依赖性机制，以促进肿瘤发生。
Cutaneous papillomaviruses are oncogenic viruses that cause severe, persistent infections that can develop into skin cancers within ultraviolet (UV)-exposed skin of immunodeficient individuals, such as those with X-linked severe combined immunodeficiency (XSCID). A canine research model of XSCID exhibits a similar phenotype; these dogs develop severe canine papillomavirus 2 (CPV2) infections that often progress to cancer. Thus, the dog is a natural, spontaneous model to investigate cutaneous papillomavirus infections in immunodeficient patients. The human papillomavirus oncogene E6 contributes to cancer development, in part, by initiating degradation of the tumor suppressor protein p53, or by inhibiting upregulation of p53-dependent genes required within the cell growth arrest and apoptotic pathways, thereby leading to an accumulation of DNA damage required for oncogenesis. Currently, little is known about CPV2, and how it promotes cancer development. The aim of this study was to determine if CPV2 oncogene E6 similarly affects p53 upon activation by UV radiation, as well as the downstream p53-regulated genes necessary to control growth arrest and apoptosis. We determined that cutaneous CPV2 E6 does not degrade p53, or interfere with the upregulation of p53-regulated genes p21, Bax, Bak, or lncRNA-p21, suggesting that CPV2 may use a p53-independent mechanism to contribute to oncogenesis.
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