The autonomous growth of human papillomavirus type 16-immortalized keratinocytes is related to the endothelin-1 autocrine loop.

摘要: Some human papillomaviruses (HPVs) such as HPV type 16 (HPV16) and HPV18 are involved in cervical carcinoma, they can immortalize transform keratinocytes. Endothelin-1 (ET-1) is produced keratinocytes has been shown to act through ETA receptors an autocrine growth factor for This study examines whether HPV16 alters the ET-1-mediated loop keratinocytes, providing a selective advantage transformed cells. ET-1 released similar amounts from normal HPV-transfected All cell lines express high-affinity receptors. A two-fold increase binding sites present HPV16-immortalized this effect seems be linked overexpression of mRNA receptor rather than differences surface/internalized ratio induces significant increases [3H]thymidine incorporation proliferation. Furthermore, proliferate absence any added medium, antagonist BQ123 prevents These data suggest new mechanism control HPV-transformed cells mediated by upregulation loop.