Table 1.
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.