Heparin-degrading sulfatases in hepatocellular carcinoma: roles in pathogenesis and therapy targets

التفاصيل البيبلوغرافية
العنوان: Heparin-degrading sulfatases in hepatocellular carcinoma: roles in pathogenesis and therapy targets
المؤلفون: Jinping Lai, James R. Thompson, Dalbir S. Sandhu, Lewis R. Roberts
المصدر: Future Oncology. 4:803-814
بيانات النشر: Future Medicine Ltd, 2008.
سنة النشر: 2008
مصطلحات موضوعية: MAPK/ERK pathway, Cancer Research, Cell growth, Cell, General Medicine, Biology, HCCS, Glypican 3, digestive system diseases, medicine.anatomical_structure, Oncology, SULF1, Cancer research, medicine, Signal transduction, neoplasms, Protein kinase B
الوصف: Hepatocellular carcinoma (HCC) is often diagnosed at an advanced stage for which there are limited treatment options. Two recently identified human heparin-degrading endosulfatases, named sulfatase 1 (SULF1) and sulfatase 2 (SULF2), have been found to be involved in liver carcinogenesis. SULF1 and SULF2 desulfate cell surface and extracellular matrix heparan sulfate proteoglycans (HSPGs) and modulate heparin-binding growth factor signaling in multiple cancers, including HCCs. SULF1 inhibits HCC tumor cell growth in vitro and in nude mice in vivo, partially through effects on gene expression mediated through histone H4 acetylation. While SULF1 is downregulated in the majority of HCC cell lines and approximately 30% of primary HCCs, SULF2 is up regulated in almost all HCC cell lines and in 60% of primary HCCs. In contrast to the tumor suppressor effect of SULF1, expression of SULF2 activates mitogen activated protein kinase (MAPK) and Akt pathways, promotes HCC cell growth in vitro and in vivo, and is associated with decreased survival of HCC patients. Targeting SULF2 or the interaction between SULF2 and SULF1 may lead to novel therapeutics for the treatment of HCCs.
تدمد: 1744-8301
1479-6694
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::0a307b5f5369b99b92162bb246e4cb49Test
https://doi.org/10.2217/14796694.4.6.803Test
حقوق: OPEN
رقم الانضمام: edsair.doi...........0a307b5f5369b99b92162bb246e4cb49
قاعدة البيانات: OpenAIRE