Đukić Anamaria, Lulić Lucija, Thomas Miranda, Skelin Josipa, Bennett Saidu Nathaniel Edward, Grce Magdalena, Banks Lawrence, Tomaić Vjekoslav
Division of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, 10000 Zagreb, Croatia.
International Centre for Genetic Engineering and Biotechnology, AREA Science Park, Padriciano 99, I-34149 Trieste, Italy.
Pathogens. 2020 Feb 18;9(2):133. doi: 10.3390/pathogens9020133.
Human papillomavirus (HPV) E6 and E7 oncoproteins are critical for development and maintenance of the malignant phenotype in HPV-induced cancers. These two viral oncoproteins interfere with a plethora of cellular pathways, including the regulation of cell cycle and the control of apoptosis, which are critical in maintaining normal cellular functions. E6 and E7 bind directly with certain components of the Ubiquitin Proteasome System (UPS), enabling them to manipulate a number of important cellular pathways. These activities are the means by which HPV establishes an environment supporting the normal viral life cycle, however in some instances they can also lead to the development of malignancy. In this review, we have discussed how E6 and E7 oncoproteins from alpha and beta HPV types interact with the components of the UPS, and how this interplay contributes to the development of cancer.
人乳头瘤病毒(HPV)E6和E7癌蛋白对于HPV诱导的癌症中恶性表型的发展和维持至关重要。这两种病毒癌蛋白会干扰大量细胞途径,包括细胞周期调控和细胞凋亡控制,而这些对于维持正常细胞功能至关重要。E6和E7直接与泛素蛋白酶体系统(UPS)的某些组分结合,使其能够操纵许多重要的细胞途径。这些活动是HPV建立支持正常病毒生命周期环境的方式,然而在某些情况下,它们也可能导致恶性肿瘤的发生。在本综述中,我们讨论了α和β型HPV的E6和E7癌蛋白如何与UPS的组分相互作用,以及这种相互作用如何促进癌症的发展。