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Targeting PBK/TOPK decreases growth and survival of glioblastoma stem cells in vitro and attenuates tumor growth in vivo

ABSTRACT: Gene knockdown of PBK led to decreased proliferation and sphere formation in the GSC cultures. Treatment of cells with different concentrations of HI-TOPK-032 almost completely abolished growth and proliferation and elicited a large increase in apoptosis

ORGANISM(S): Homo sapiens

PROVIDER: GSE53800 | GEO | 2015/06/16

SECONDARY ACCESSION(S): PRJNA233313

REPOSITORIES: GEO

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Targeting PBK/TOPK decreases growth and survival of glioblastoma stem cells in vitro and attenuates tumor growth in vivo

Project description:Gene knockdown of PBK led to decreased proliferation and sphere formation in the GSC cultures. Treatment of cells with different concentrations of HI-TOPK-032 almost completely abolished growth and proliferation and elicited a large increase in apoptosis Total RNA isolated from GSC cultures featuring PBK gene knock-down (shRNA) was compared to that from non-silencing control GSC cultures (NS-shRNA). Total RNA isolated from GSC cultures treated with PBK-inhibitor was compared to that from untreated GSC cultures.

2015-06-16 | E-GEOD-53800 | biostudies-arrayexpress

Effect of PDZ domain binding Kinase inhibition using TOPK-32 (called PBKi) on C4-2 cell transcriptome

Project description:Analysis of C4-2 prostate cancer cell line after 6 hrs of treatment with TOPK-32. PBK is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of PBK in prostate carcinogenesis.

2018-08-30 | GSE64341 | GEO

PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites

Project description:PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in Pbk–/– preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by Ikzf1, Ikzf3, Znf131 and Zbtb11. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction.

2025-07-21 | GSE266554 | GEO

Knockdown of NAT12/NAA30 decreases glioblastoma stem cell growth and tumorigenicity by regulating hypoxia response, p-MTOR (Ser2448) and p53 pathway

Project description:Gene knockdown of NAT12/NAA30 led to decreased proliferation, sphere forming ability and mitochondrial hypoxia tolerance in the GSC T65 culture. Intracranial transplantation of these cells into SCID mice showed that the decreased NAT12/NAA30 expression correlated with the prolonged animal survival and reduced tumor size Total RNA isolated from GSC cultures featuring NAT12/NAA30 gene knock-down (shRNA) was compared to total RNA from non-silencing control GSC cultures (NS-shRNA).

2015-11-23 | E-GEOD-60706 | biostudies-arrayexpress

PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites

2025-07-21 | PXD057894 | Pride

PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites

2025-07-21 | PXD057898 | Pride

Knockdown of NAT12/NAA30 decreases glioblastoma stem cell growth and tumorigenicity by regulating hypoxia response, p-MTOR (Ser2448) and p53 pathway

2015-11-23 | GSE60706 | GEO

RNA-seq of Hacat cells treated with TOPK inhibitor

Project description:Hacat cells were treated with TOPK inhibitor to elucidate the effect of TOPK signaling on Hacat cells

2024-01-18 | GSE253203 | GEO

Targeting PBK/TOPK decreases growth and survival of glioma initiating cells in vitro and attenuates tumor growth in vivo.

Project description:BackgroundGlioblastomas are invasive therapy resistant brain tumors with extremely poor prognosis. The Glioma initiating cell (GIC) population contributes to therapeutic resistance and tumor recurrence. Targeting GIC-associated gene candidates could significantly impact GBM tumorigenicity. Here, we investigate a protein kinase, PBK/TOPK as a candidate for regulating growth, survival and in vivo tumorigenicity of GICs.MethodsPBK is highly upregulated in GICs and GBM tissues as shown by RNA and protein analyses. We knocked down PBK using shRNA vectors and inhibited the function of PBK protein with a pharmacological PBK inhibitor, HITOPK-032. We assessed viability, tumorsphere formation and apoptosis in three patient derived GIC cultures.ResultsGene knockdown of PBK led to decreased viability and sphere formation and in one culture an increase in apoptosis. Treatment of cells with inhibitor HITOPK-032 (5 μM and 10 μM) almost completely abolished growth and elicited a large increase in apoptosis in all three cultures. HI-TOPK-032 treatment (5 mg/kg and 10 mg/kg bodyweight) in vivo resulted in diminished growth of experimentally induced subcutaneous GBM tumors in mice. We also carried out multi-culture assays of cell survival to investigate the relative effects on GICs compared with the normal neural stem cells (NSCs) and their differentiated counterparts. Normal NSCs seemed to withstand treatment slightly better than the GICs.ConclusionOur study of identification and functional validation of PBK suggests that this candidate can be a promising molecular target for GBM treatment.

| S-EPMC4470057 | biostudies-literature

Gene knockdown of PBK in the glioblastoma stem-like cell (GSC) culture T59

Project description:Expression of genes in the GSC culture T59 featuring PBK gene knockdown. Expression of genes in the GSC culture T59 over-expressing non-silencing (NS-shRNA) transgenic sequence.

2021-03-05 | GSE60704 | GEO

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