» Articles » PMID: 25325976

Measuring Sulfatase Expression and Invasion in Glioblastoma

Overview
Specialty Molecular Biology
Date 2014 Oct 19
PMID 25325976
Citations 6
Authors
Affiliations
Soon will be listed here.
Abstract

Extracellular sulfatases (SULF1 and SULF2) selectively remove 6-O-sulfate groups from heparan sulfate proteoglycans (HSPGs) and by this process control important interactions of HSPGs with extracellular factors including morphogens, growth factors, and extracellular matrix components. The expression of SULF1 and SULF2 is dynamically regulated during development and is altered in pathological states such as glioblastoma (GBM), a highly malignant and highly invasive brain cancer. SULF2 protein is increased in an important subset of human GBM and it helps regulate receptor tyrosine kinase signaling and tumor growth in a murine model of the disease. By altering ligand binding to HSPGs, SULF2 has the potential to modify the extracellular availability of factors important in a number of cell processes including proliferation, chemotaxis, and migration. Diffuse invasion of malignant tumor cells into surrounding healthy brain is a characteristic feature of GBM that makes therapy challenging. Here, we describe methods to assess SULF2 expression in human tumor tissue and cell lines and how to relate this to tumor cell invasion.

Citing Articles

Sulfatase 2 Affects Polarization of M2 Macrophages through the IL-8/JAK2/STAT3 Pathway in Bladder Cancer.

Zhang W, Yang F, Zheng Z, Li C, Mao S, Wu Y Cancers (Basel). 2023; 15(1).

PMID: 36612128 PMC: 9818157. DOI: 10.3390/cancers15010131.


In-Depth Matrisome and Glycoproteomic Analysis of Human Brain Glioblastoma Versus Control Tissue.

Sethi M, Downs M, Shao C, Hackett W, Phillips J, Zaia J Mol Cell Proteomics. 2022; 21(4):100216.

PMID: 35202840 PMC: 8957055. DOI: 10.1016/j.mcpro.2022.100216.


SULF2 promotes tumorigenesis and inhibits apoptosis of cervical cancer cells through the ERK/AKT signaling pathway.

Jiang T, Chen Z, Chen Z, Tan D Braz J Med Biol Res. 2020; 53(2):e8901.

PMID: 32049100 PMC: 7006129. DOI: 10.1590/1414-431X20198901.


Mechanisms of Resistance to EGFR Inhibition Reveal Metabolic Vulnerabilities in Human GBM.

McKinney A, Lindberg O, Engler J, Chen K, Kumar A, Gong H Mol Cancer Ther. 2019; 18(9):1565-1576.

PMID: 31270152 PMC: 6726545. DOI: 10.1158/1535-7163.MCT-18-1330.


Heparan Sulfate Glycosaminoglycans in Glioblastoma Promote Tumor Invasion.

Tran V, Wade A, McKinney A, Chen K, Lindberg O, Engler J Mol Cancer Res. 2017; 15(11):1623-1633.

PMID: 28778876 PMC: 6059807. DOI: 10.1158/1541-7786.MCR-17-0352.


References
1.
Bernfield M, Gotte M, Park P, Reizes O, Fitzgerald M, Lincecum J . Functions of cell surface heparan sulfate proteoglycans. Annu Rev Biochem. 2000; 68:729-77. DOI: 10.1146/annurev.biochem.68.1.729. View

2.
Dhoot G, Gustafsson M, Ai X, Sun W, Standiford D, EMERSON Jr C . Regulation of Wnt signaling and embryo patterning by an extracellular sulfatase. Science. 2001; 293(5535):1663-6. DOI: 10.1126/science.293.5535.1663. View

3.
Fujita K, Takechi E, Sakamoto N, Sumiyoshi N, Izumi S, Miyamoto T . HpSulf, a heparan sulfate 6-O-endosulfatase, is involved in the regulation of VEGF signaling during sea urchin development. Mech Dev. 2009; 127(3-4):235-45. DOI: 10.1016/j.mod.2009.12.001. View

4.
Morimoto-Tomita M, Uchimura K, Bistrup A, Lum D, Egeblad M, Boudreau N . Sulf-2, a proangiogenic heparan sulfate endosulfatase, is upregulated in breast cancer. Neoplasia. 2005; 7(11):1001-10. PMC: 1502017. DOI: 10.1593/neo.05496. View

5.
Calvo F, Sahai E . Cell communication networks in cancer invasion. Curr Opin Cell Biol. 2011; 23(5):621-9. DOI: 10.1016/j.ceb.2011.04.010. View