Table 1.

Main findings on the role of the primary cilium in glioblastoma.

Year	Finding	Reference(s)
2009	First report of aberrant/failed ciliogenesis in human GBM cell lines	Moser et al.54
2013	Primary cilia loss via CDK20/CCRK overexpression promotes GBM proliferation in U-251 MG cells, which could be partially mediated by aberrant activation of the PI3K pathway	Yang et al.60
2014	Ciliogenesis is also disrupted in human GBM tumours	Moser et al.55
2014	Small subpopulations of cells in GBM tumours are ciliated and co-stain with Ki-67 and ZEB1	Sarkisian et al.56
2014	Ciliary gene expression patterns are downregulated in GBM	Shpak et al.57
2016	Primary cilium is able to modulate GBM proliferation through Shh signalling in patient-derived GBM cell lines, in a cell-line specific manner	Hoang-Minh et al.65
2016	Reduced ciliogenesis via PCM1 depletion decreases proliferation and increases sensitivity to TMZ in patient-derived GBM cell lines	Hoang-Minh et al.66
2018	Primary cilia loss is required to maintain highly proliferative phenotypes in patient-derived GBM cell lines by modulating LPA-mediated signalling	Loskutov et al.62

CDK20/CCRK, cyclin-dependent kinase 20/cell-cycle related kinase; GBM, glioblastoma; LPA, lysophosphatidic acid; PCM1, pericentriolar material 1; PI3K, phosphatidylinositol-3-kinase; Shh, Sonic hedgehog; TMZ, temozolomide; ZEB1, zinc finger E-box binding homeobox.