High-risk human papillomavirus type 18 E7 caused p27 elevation and cytoplasmic localization

The tumor suppressor p27^Kip1 is an inhibitor of cyclin/cyclin-dependent kinase (CDK) complexes and plays a crucial role in cell cycle regulation. Nevertheless, p27 function in the tumorigenesis of the uterine cervix has been poorly defined. Some phenomenon hints that HPV E7 protein can enhance p27 expression, which is contradictory to HPV E7's property of increasing cell proliferation rate. So, in the present study, we have examined the effect of E7 on p27 expression. Though the levels of p27 are increased after HPV E7 expression, most of the p27 protein localized in the cytoplasm and have no function on cell cycle arrest and contact inhibition. The cell migration rate is elevated when p27 is high expression and located in cytoplasm. The results indicated that e7-p27 interaction not only abolished the p27's cell cycle inhibitory function by sequestering it to the cytoplasm, but also endow the cell with invasive property which is the feature of malignant cells.