Atta-Ur-Rahman School of Applied Biosciences, National University of Science and Technology, H-12 Campus, Islamabad, Pakistan.
Microb Pathog. 2020 Feb;139:103923. doi: 10.1016/j.micpath.2019.103923. Epub 2019 Dec 11.
Oncoprotein E5 is gaining popularity with time as the third transforming protein of Human Papillomavirus (HPV). Extensive proliferation is the distinguished feature of developing cancers, and E5 is able to stimulate keratinocytes proliferation via upregulation of EGFR signaling pathway. Thus E5 is thought to indirectly contribute to the completion of the viral life-cycle by generating the adequate cellular environment. By amplifying EGFR signaling E5 delays differentiation and allows hyperproliferation of keratinocytes which otherwise would have followed a normal differentiation pathway. Thus exploring the mechanisms by which HPV E5 regulates signaling by EGFR receptors in detail suggest new ways of inhibiting HPV-mediated disease progression.
癌蛋白 E5 随着时间的推移逐渐受到关注，成为人乳头瘤病毒 (HPV) 的第三种转化蛋白。广泛增殖是癌症发展的显著特征，E5 能够通过上调 EGFR 信号通路刺激角质形成细胞增殖。因此，E5 被认为通过产生足够的细胞环境间接促进病毒生命周期的完成。通过放大 EGFR 信号，E5 延迟角质形成细胞的分化，并允许其过度增殖，否则这些细胞将遵循正常的分化途径。因此，详细研究 HPV E5 如何调节 EGFR 受体信号转导的机制，为抑制 HPV 介导的疾病进展提供了新的途径。
