International Centre for Genetic Engineering and Biotechnology, Padriciano 99, I-34149, Trieste, Italy.
International Centre for Genetic Engineering and Biotechnology, Padriciano 99, I-34149, Trieste, Italy; Dana-Farber Cancer Institute, 450 Brookline Avenue, Mayer 440, Boston, MA, 02215, USA.
Tumour Virus Res. 2024 Jun;17:200279. doi: 10.1016/j.tvr.2024.200279. Epub 2024 Mar 12.
Multiple cellular pathways are affected by HPV E6 and E7 oncoproteins, including endocytic and cellular trafficking. HPV-16 E7 can target the adaptor protein (AP) complex, which contains proteins important during endocytosis transport. To further investigate the role of HPV E7 during this process, we analysed the expression of cell surface proteins in NIKS cells expressing HPV-16 E7. We show that different cell surface proteins are regulated by HPV-16 E7 via interaction with AP2. We observed that the expression of MET and CD109 membrane protein seems to be upregulated in cells expressing E7. Moreover, the interaction of MET and CD109 with AP2 proteins is disrupted by HPV-16 E7. In addition, in the absence of HPV-16 E7, there is a downregulation of the cell membrane expression of MET and CD109 in HPV-positive cell lines. These results expand our knowledge of the functions of E7 and open new potential cellular pathways affected by this oncoprotein.
多种细胞途径受到 HPV E6 和 E7 癌蛋白的影响,包括内吞作用和细胞运输。HPV-16 E7 可以靶向衔接蛋白 (AP) 复合物,该复合物包含内吞作用运输过程中重要的蛋白质。为了进一步研究 HPV E7 在这个过程中的作用,我们分析了表达 HPV-16 E7 的 NIKS 细胞表面蛋白的表达。我们发现不同的细胞表面蛋白通过与 AP2 的相互作用被 HPV-16 E7 调控。我们观察到表达 E7 的细胞中 MET 和 CD109 膜蛋白的表达似乎上调。此外,HPV-16 E7 破坏了 MET 和 CD109 与 AP2 蛋白的相互作用。此外,在没有 HPV-16 E7 的情况下,HPV 阳性细胞系中 MET 和 CD109 的细胞膜表达下调。这些结果扩展了我们对 E7 功能的认识,并为受这种癌蛋白影响的新的潜在细胞途径开辟了道路。