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Literature summary for 2.8.2.29 extracted from

  • Denys, A.; Allain, F.
    The emerging roles of heparan sulfate 3-O-sulfotransferases in cancer (2019), Front. Oncol., 9, 507 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.8.2.29

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine Homo sapiens
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 adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens Q9Y278
-
-

Source Tissue

Source Tissue Comment Organism Textmining
cerebellum
-
 Homo sapiens
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cerebral cortex high expression level Homo sapiens
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colon
-
 Homo sapiens
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lung
-
 Homo sapiens
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additional information isozyme HS3ST2 is not expressed in cell lines representative of the different molecular breast cancer subgroups Homo sapiens
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placenta
-
 Homo sapiens
-
small intestine
-
 Homo sapiens
-
spleen
-
 Homo sapiens
-
stomach
-
 Homo sapiens
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testis
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
-
 Homo sapiens adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
 ?

Synonyms

Synonyms Comment Organism
heparan sulfate 3-O-sulfotransferase
-
 Homo sapiens
HS3ST2
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens expression of the genes encoding HS-modifying enzymes is frequently dysregulated in cancer and other diseases additional information

General Information

General Information Comment Organism
evolution HS3STs represent the largest family of HS-modifying enzymes, and yet the reaction of 3-O-sulfation is the rarest maturation step, when compared to other sulfations. Seven HS3STs have been characterized in human, for which the expression is dependent on cell type and tissue environment Homo sapiens
malfunction expression of the genes encoding HS-modifying enzymes is frequently dysregulated in cancer and other diseases. The enzymes show either anti-oncogenic or tumor-promoting effects. The 5' region of the HS3ST2 gene is hypermethylated in tumor tissue but not in surrounding non-cancerous tissue. The expression level of HS3ST2 is markedly reduced in the cancer sample compared with the matched normal counterpart. Reversing methylation restores the expression of the enzyme, confirming the silencing effect of gene methylation. Moreover, HS3ST2 gene hypermethylation is detected in the majority of primary breast cancer samples analysed, and also in human colon, lung and pancreatic cancers. Hypermethylation s found at high frequency in gastric, breast, colorectal, prostate and cervix cancers, as well as in hematological neoplasms. In breast and cervix, hypermethylation of the HS3ST2 gene occurs early during malignant transformation, suggesting a correlation between HS3ST2 silencing and progression of the disease. The exogenous reexpression of HS3ST2 is efficient to inhibit cell migration, invasion and proliferation in various lung cancer cell lines. But the tumor size is not significantly different between patients with HS3ST2 gene hypermethylation and those without, in spite of the anti-proliferative property of HS3ST2 observed in vitro. Re-expression of HS3ST2 in MDA-MB-231 cells leads to an increase in cell viability and invasion, MDA-MB-231 cells carrying HS3ST2 expression display a significant increase in proliferation and survival Homo sapiens
metabolism HS3ST-mediated 3-O-sulfation leads to at least two distinct forms of 3-O-sulfated motifs. HS3ST1 and HS3ST5 participate in the generation of anticoagulant-active HS/heparin sequences for antithrombin-III, while HS3ST2, HS3ST3A, HS3ST3B, HS3ST4, and HS3ST6 are described to provide the HS-binding motifs for the glycoprotein gD of herpes simplex virus-1 (HSV-1). HS3ST regulations in cancer cells, cell proliferation, and tumor progression, overview Homo sapiens
additional information to date, only a few ligands are known to selectively interact with 3-O-sulfated motifs, whereas hundreds of HS-binding proteins have been identified Homo sapiens
physiological function isozymes HS3ST2, HS3ST3B, and HS3ST4 may exhibit a broader selectivity. Re-expression of HS3ST2 in MDA-MB-231 cells leads to an increase in cell viability and invasion, MDA-MB-231 cells carrying HS3ST2 expression display a significant increase in proliferation and survival. Consistent with a proinvasive phenotype, Erk1/2 and beta-catenin signalling is upregulated in HS3ST2-expressing cells in an HS-dependent manner. The tumor-promoting effects of HS3ST2, HS3ST3B, and HS3ST4 are related to sustained activation of Src, Akt, and NF-kappaB, and upregulation of the anti-apoptotic proteins survivin and XIAP. Importantly, all these signalling molecules have been well described to play a critical role in promoting tumor growth and resistance to apoptosis Homo sapiens