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• W3093793735 abstract "Primary cilia are highly conserved eukaryotic organelles that serve as a ‘’cellular antenna’’ forsignaling functions. Dysfunctions or defects in primary cilia are associated with numerous humandiseases. Typically, the mother centriole, transforms into a structure called basal body, which thentemplates the formation of the primary cilium. Abnormal cilia are implicated in cancer progressionssuch as in breast, pancreatic, brain, and prostate cancers. Glioblastoma multiforme (GBM) is one ofthe most frequent lethal primary brain tumors.GBM is characterized by extreme heterogeneity, rapid growth, and efficient invasion of neoplasticcells, called Glioblastoma Stem-like Cells (GSCs). GSCs represent a subpopulation of the cells thatare resistant to treatment and are suspected to be driving forces for the disease recurrence. Untilnow, there is no effective treatment for GBM. The average median survival time of the patients fromthe initial diagnosis is 12-15 months. GBM cells appear to lose cilia, which can contribute to themalignant phenotype. However, the mechanism of suppressed ciliogenesis is not fully characterizedyet. Thus, the aims of this thesis were (i) to understand the possible mechanisms that can suppressthe ciliogenesis in GSCs, (ii) to investigate the pathways that could restore the ciliogenesis and, (iii)characterize GSCs after cilium induction.Primary cilium assembly and disassembly are a dynamic process, which is coupled with the cellcycle. At the onset of cilium disassembly, the Centrosomal-P4.1-associated protein (CPAP) providesa scaffold for the cilium-disassembly complex (CDC) proteins, including NDE1, OFD1, NEK2, andCPAP. These proteins are recruited to the ciliary base to ensure timely cilium disassembly andpromote cell cycle progression. Hence, using multidisciplinary approaches, the current doctoralthesis investigated primary cilia dynamics in multiple patient-derived GSCs. The experimentsrevealed that elevated levels and recruitment of CDC components lead to suppressing of theciliogenesis and an increase in the cell cycle progression.Moreover, depletion of different CDC proteins induced ciliogenesis in GSCs in which PDGFR-α levelis elevated. Among the CDC proteins, NEK2 depletion induced the maximum frequencies of ciliationin GSCs. Furthermore, inducible overexpression of the catalytically inactive NEK2 in GSCs wassufficient to induce cilia irreversibly. Importantly, both functional, including transcriptomic analyzes,showed that cilium induction switched GSCs from self-renewal to differentiation state. Takentogether, the current work provides evidence for a novel mechanism to induce ciliogenesis in patient-derivedGSCs and suggests that the cilium induction can potentially serve as a new strategy tointervene in GSCs proliferation." @default.
• W3093793735 created "2020-10-29" @default.
• W3093793735 creator A5006358536 @default.
• W3093793735 date "2020-09-22" @default.
• W3093793735 modified "2023-09-27" @default.
• W3093793735 title "Characterization of primary cilia in patient-derived glioma stem cells" @default.
• W3093793735 hasPublicationYear "2020" @default.
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