Tie1 derived from cervical cancer promotes the invasion and metastasis by Ang1 mediating Tie2/PI3K/Akt signaling axis and angiogenesis.

Tie1, an orphan receptor, is a receptor tyrosine kinase that is expressed in endothelial cells. It can form a polymer with Tie2, thereby regulating the Ang/Tie2 signaling pathway, which is crucial for angiogenesis and plays a significant role in tumor progression. However, the specific role of Tie1, particularly in tumor processes, remains poorly understood. In this study, we investigated the functional effects of Tie1 knockdown in cervical cancer both in vitro and in vivo. We used CCK-8, wound healing, and Transwell assays to evaluate cervical cancer cell proliferation and migration in vitro. Additionally, we established subcutaneous xenograft tumor and lung metastasis mouse models to examine tumor growth and metastasis. The impact of Tie1 knockdown cervical cancer cell-conditioned medium on human umbilical vein endothelial cell (HUVEC) angiogenesis was assessed using an angiogenesis assay. Tie1 knockdown inhibited activation of the Tie2/PI3K/Akt signaling axis and weakened the migration and invasion abilities of cervical cancer cells in vitro and in vivo. Addition of Ang1 partially reversed the effects of Tie1 knockdown. Knockdown of Tie1 also reduces CD31 protein expression in vitro and in vivo. Tie1 derived from cervical cancer cells exerts an oncogenic role by promoting progression through activation of the Ang1/Tie2/PI3K/Akt signaling axis. These findings may provide new biomarkers and identify potential therapeutic targets for cervical cancer.