Home HOME Neoplasma 2010 Neoplasma Vol.57, No.6, p.562-571, 2010

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.57, No.6, p.562-571, 2010

Title: Heparanase participates in the growth and invasion of human U-2OS osteosarcoma cells and its close relationship with hypoxia-inducible factor-1α in osteosarcoma
Author: C. ZENG Z. KE, C. LUO, Z. YANG, L. WANG

Abstract:

Although the expression of heparanase is associated with invasion and metastasis of various human cancers, the effects of heparanase on human osteosarcoma have not been evaluated. We showed that down-regulating the expression of heparanase significantly reduced proliferation and invasion of human U-2OS osteosarcoma cells. Furthermore, heparanase silencing by short-hairpin RNA (shRNA) was associated with decreased hypoxia-inducible factor-1α (HIF-1α) level, implying that heparanase was associated with the expression of HIF-1α. This result was confirmed by immunohistochemistry analysis. In osteosarcoma tissues, immunohistochemical results revealed that heparanase expression had a close correlation with that of HIF-1α and they had a strong relation with presence of pulmonary metastasis (P<0.05).
Heparanase-positive samples had higher microvessel density (MVD) than heparanase-negative samples. Similarly, compared with HIF-1α-negative samples, HIF-1α-positive samples had higher MVD. Therefore, heparanase and HIF-1α facilitated tumor angiogenesis and promoted pulmonary metastasis of osteosarcoma.



Keywords: heparanase, HIF-1α, osteosarcoma, invasion, angiogenesis
Year: 2010, Volume: 57, Issue: 6 Page From: 562, Page To: 571
doi:10.4149/neo_2010_06_562


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.