Home Neoplasma 2013 Neoplasma Vol.60, No.1, p.41-45, 2013

Journal info


6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.60, No.1, p.41-45, 2013

Title: Targeting rictor inhibits mouse vascular tumor cell proliferation and invasion in vitro and tumor growth in vivo
Author: N. N. ZHENG, X. D. DING, H. P. ZHANG

Abstract: Vascular tumor is an abnormal buildup of blood vessels in the skin or internal organs that can lead to disfigurement and/or life-threatening consequences. The mechanism of hemangiogenesis remains unknown. The aim of this study was to assess the role of rapamycin-insensitive companion of mTOR (Rictor) in control of vascular tumor malignant biological behavior and cell signaling mechanism in Mouse Hemangioendothelioma Endothelial Cells (EOMA cells) and nude mouse model. Knocking down rictor was mediated by lentivirus shRNA. The role and mechanism of rictor in vascular tumor were assessed by western blotting, wst-1 proliferation assay, matrigel invasion assay and xenograft vascular tumor growth. Our results in vitro showed that loss of rictor down-regulated phosphorylation of AKT and S6 by which EOMA cells growth and proliferation were greatly suppressed. Knock down of rictor also inhibited the invasion of EOMA cells. Furthermore, we demonstrated that knock down of rictor inhibited xenograft vascular tumor growth in nude mice. Taken together, we purpose that rictor contributed to vascular tumor growth and progression. Targeting rictor becomes an effective strategy in vascular tumor treatment.

Keywords: AKT, mTOR2, rictor, vascular tumor, hemangioma
Year: 2013, Volume: 60, Issue: 1 Page From: 41, Page To: 45
doi:10.4149/neo_2013_006


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.