GPC2 is highly expressed in about half of neuroblastoma cases and that high GPC2 expression correlates with poor overall survival, suggesting GPC2 as a therapeutic target in neuroblastoma.[5][6] GPC2 silencing inactivates Wnt/β-catenin signaling and reduces the expression of N-Myc, an oncogenic driver of neuroblastoma tumorigenesis. Immunotoxins and chimeric antigen receptor (CAR) T cells targeting GPC2 inhibit neuroblastoma growth in mouse models.[5]
↑Ivins JK, Litwack ED, Kumbasar A, Stipp CS, Lander AD (April 1997). "Cerebroglycan, a developmentally regulated cell-surface heparan sulfate proteoglycan, is expressed on developing axons and growth cones". Developmental Biology. 184 (2): 320–32. doi:10.1006/dbio.1997.8532. PMID9133438.
↑Herndon ME, Stipp CS, Lander AD (February 1999). "Interactions of neural glycosaminoglycans and proteoglycans with protein ligands: assessment of selectivity, heterogeneity and the participation of core proteins in binding". Glycobiology. 9 (2): 143–55. doi:10.1093/glycob/9.2.143. PMID9949192.
↑Bosse KR, Raman P, Zhu Z, Lane M, Martinez D, Heitzeneder S, et al. (September 2017). "Identification of GPC2 as an Oncoprotein and Candidate Immunotherapeutic Target in High-Risk Neuroblastoma". Cancer Cell. 32 (3): 295–309.e12. doi:10.1016/j.ccell.2017.08.003. PMID28898695.
