Qki deficiency maintains stemness of glioma stem cells in suboptimal environment by downregulating endolysosomal degradation.

ABSTRACT: Stem cells, including cancer stem cells (CSCs), require niches to maintain stemness, yet it is unclear how CSCs maintain stemness in the suboptimal environment outside their niches during invasion. Postnatal co-deletion of Pten and Trp53 in mouse neural stem cells (NSCs) leads to the expansion of these cells in their subventricular zone (SVZ) niches but fails to maintain stemness outside the SVZ. We discovered that Qki is a major regulator of NSC stemness. Qk deletion on a Pten^-/-; Trp53^-/- background helps NSCs maintain their stemness outside the SVZ in Nes-CreER^T2; Qk^L/L; Pten^L/L; Trp53^L/L mice, which develop glioblastoma with a penetrance of 92% and a median survival time of 105 d. Mechanistically, Qk deletion decreases e

SUBMITTER: Shingu T 

PROVIDER: S-EPMC5453714 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature