EC Number |
Expression |
Reference |
---|
3.2.1.166 | down |
the overall transcriptional activity of the main heparan sulfate biosynthesis-involved genes (EXT1, EXT2, NDST1, NDST2, GLCE, HS2ST1, HS3ST1, HS3ST2, HS6ST1, HS6ST2, SULF1, SULF2, HPSE) is decreased by 1.5-2fold in Grade II-III glioma (p < 0.01) and by 3-fold in Grade IV glioma (glioblastoma multiforme, GBM) (p < 0.05), as compared with the para-tumourous tissue |
759360 |
3.2.1.166 | more |
no effect by TGF-beta on the enzyme expression in enzyme-silenced cells |
731355 |
3.2.1.166 | up |
bovine serum albumin and advanced glycation end-product, but not high glucose levels, increase heparanase expression in adult tubular cells via the AKT/PI3K signaling pathway 1.68 and 2.81times, respectively |
714343 |
3.2.1.166 | up |
expression is up-regulated as tumors become more aggressive and is associated with enhanced tumor growth, angiogenesis, and metastasis |
732087 |
3.2.1.166 | up |
expression of the enzyme heparanase is clearly linked to colon carcinoma progression |
715737 |
3.2.1.166 | up |
heparanase expression is enhanced in almost all cancers examined including various carcinomas, sarcomas and hematological malignancies. Upregulation of heparanase expression correlates with increased tumor size, tumor angiogenesis, enhanced metastasis and poor prognosis. Heparanase is upregulated in response to chemotherapy in cancer patients and the surviving cells acquire chemoresistance, attributed, at least in part, to autophagy |
753404 |
3.2.1.166 | up |
heparanase expression is induced by nerve growth factor |
714108 |
3.2.1.166 | up |
heparanase is up-regulated in essentially all human tumors examined. Oxidized lipid- or angiotensin-induced expression of heparanase in macrophages may be a primary mechanism increasing heparanase in atherosclerotic plaques |
732437 |
3.2.1.166 | up |
heparanase is upregulated in essentially all human carcinomas |
714960 |
3.2.1.166 | up |
heparanase is upregulated in primary human tumors |
714922 |