Taken together with the recent demonstration of the involvement of MIAT in glioblastoma, our observations suggest that MIAT could possess tumour-promoting properties, thereby acting as an oncogene, and has the potential to be used as a reliable biomarker for neuroblastoma and glioblastoma and be employed for prognostic, predictive and, potentially, therapeutic purposes for these cancers.
Here we show that both increases and decreases in GPR124 expression in glioblastoma cells reduce cell proliferation by differentially altering the duration mitotic progression.
Hyperphosphorylation of CDH1 in Glioblastoma Cancer Stem Cells Attenuates APC/C<sup>CDH1</sup> Activity and Pharmacologic Inhibition of APC/C<sup>CDH1/CDC20</sup> Compromises Viability.
50 glioblastoma samples were stained with two custom-made antibodies against LuzP6 and commercial antibodies against ApoC1, C12orf75 and OCC-1 and analyzed.
Further, we also revealed that NUCB2 promoted cell proliferation and invasion of glioblastoma <i>in vitro</i> and promoted the growth and metastasis of glioblastoma in mice.
GABPA depletion or the disruption of the GABPA/GABPB1 complex by knocking down GABPB1 was shown to inhibit telomerase, thereby eliminating the tumorigenic potential of glioblastoma cells.
We confirmed that CBX3 was overexpressed in glioblastoma by immunohistochemical analysis of tissue microarrays and qPCR analysis of surgical specimens.
Interleukin-8 Secreted by Glioblastoma Cells Induces Microvascular Hyperpermeability Through NO Signaling Involving S-Nitrosylation of VE-Cadherin and p120 in Endothelial Cells.
Despite the improved pharmacokinetic profiles, D8-sLip/DOX exhibited comparable brain targeting capacity in ICR mice and antiglioblastoma efficacy to <sup>D</sup>CDX-sLip/DOX in nude mice bearing intracranial glioblastoma.