Background: Hemangiomas are common vascular endothelial cell tumors. Abnormally activated PI3K/Akt signaling pathway is one of the most important biological characteristics of Hemangioma. 3-phosphoinositide-dependent kinase 1(PDK1), an upstream protein of Akt, regulates the activity of Akt and its downstream kinases. The objective of this study is to explore the effect of PDK1 on malignant vascular tumors and their cell signaling mechanism in mice.
Methods: Mouse Hemangioendothelioma Endothelial Cells (EOMA cells) and Nu/Nu mice were used. The silencing of PDK1 was mediated by lentiviral shRNA. Western blotting, WST-1 proliferation assay, Matrigel invasion assay, and Xenograft vascular tumor model were utilized to examine the effects and mechanism of PDK1 growth, proliferation, and invasion of an Hemangioma.
Results: PDK1 deficiency significantly reduced the proliferation and invasion of EOMA cells in vitro, and depressed the growth of vascular tumor in vivo by decreasing the activity of Akt signaling pathway.
Conclusion: We hypothesize that PDK1 plays a significant role in the progression and growth of vascular tumors and targeting PDK1 may thus be considered in their treatment.
© 2015 S. Karger AG, Basel.