Targeting rictor inhibits mouse vascular tumor cell proliferation and invasion in vitro and tumor growth in vivo.

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.

• Authors: N N Zheng, X D Ding, H P Zhang
• Journal: Neoplasma (Neoplasma) Vol. 60 Issue 1 Pg. 41-5 ( 2013) ISSN: 0028-2685 [Print] Slovakia
• PMID: 23067215 (Publication Type: Journal Article)

Chemical References

• Carrier Proteins
• RICTOR protein, human
• RNA, Small Interfering
• Rapamycin-Insensitive Companion of mTOR Protein
• Phosphatidylinositol 3-Kinases
• Proto-Oncogene Proteins c-akt
• PTEN Phosphohydrolase
• PTEN protein, human

Topics

• Animals
• Apoptosis
• Blotting, Western
• Carrier Proteins (antagonists & inhibitors, genetics, metabolism)
• Cell Proliferation
• Female
• Hemangioendothelioma (metabolism, pathology, prevention & control)
• Humans
• In Vitro Techniques
• Mice
• Mice, Nude
• Neoplasm Invasiveness
• Neovascularization, Pathologic
• PTEN Phosphohydrolase (metabolism)
• Phosphatidylinositol 3-Kinases (metabolism)
• Phosphorylation
• Proto-Oncogene Proteins c-akt (metabolism)
• RNA, Small Interfering (genetics)
• Rapamycin-Insensitive Companion of mTOR Protein
• Signal Transduction
• Tumor Cells, Cultured
• Xenograft Model Antitumor Assays