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Homo sapiens

ABSTRACT: HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)

OTHER RELATED OMICS DATASETS IN: E-GEOD-56517

PROVIDER: PRJNA243617 | ENA |

REPOSITORIES: ENA

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HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)

Project description:Assess gene expression patterns upon HOXA9 ectopic expression in U87MG GBM cell line and hTERT/E6/E7 immortalized human astrocytes, and HOXA9 silencing in U251 and GBML18 GBM cell lines. U87MG and hTERT/E6/E7 were retrovirally-infected with an MSCV control vector (MSCV-Control) or with a construct containing the coding region of HOXA9 (MSCV-HOXA9), resulting in U87MG-Control, U87MG-HOXA9, hTERT/E6/E7-Control and hTERT/E6/E7-HOXA9 cell lines. GBML18 and U251 cells were transfected with HOXA9 gene-specific shRNA sequences (shHOXA9) or a non-efective shRNA (shControl) in pGFP-V-RS plasmid, resulting in U251-shControl, U251-shHOXA9, GBML18-shControl and GBML18-shHOXA9 cell lines. Four experimental replicates for HOXA9 overexpression cell lines, and three for HOXA9 silencing cell lines were performed.

2015-01-30 | E-GEOD-56517 | biostudies-arrayexpress

HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)

2015-01-30 | GSE56517 | GEO

E-GEOD-56517

Project description:HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)

2025-01-24 | E-GEOD-56517 | ExpressionAtlas

Homo sapiens immortalized MSCs: KP vs. 3A6

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Homo sapiens immortalized MSCs: 3A6

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Homo sapiens immortalized MSCs: KP vs. 3A6

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Homo sapiens immortalized MSCs: 3A6

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Amniocytes (AM) vs. Immortalized AM

Project description:Transcriptional profiling of AM (amniocytes) vs. three different immortalized AM-derived cell lines. Immortalization of AM-derived cell lines by lentiviral vector with hTERT and E6-E7.

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Proteomics of KRAS mutated and non-transformed pancreas cells treated with ethanol

Project description:The goal for this study was to determine the effects of ethanol on pancreas cells and examine how ethanol influences protein expression in non-transformed and mutant KRAS cells. We performed TMT-labeled proteomics of non-transformed (hTERT-HPNE E6/E7) and KRAS mutated (hTERT-HPNE E6/E7/K-RasG12D) human pancreas cell lines following 6 months of 100 mM ethanol treatment.

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Dysregulation of microtubule dynamics caused by LOXL3 knockout triggers mitosis catastrophe and senescence in U87MG and U251 cells

Project description:The amine oxidase LOXL3 has been implicated in tumor development and progression, with elevated expression in glioblastoma (GBM). This enzyme influences GBM cell adhesion, migration, and proliferation, and is demonstrated correlation with tubulin expression. Microtubules, as the major component of the cytoskeleton, are crucial for cell cycle and mitotic progression. In this study, LOXL3 knockout was performed using CRISPR-Cas9 in two GBM cell lines, U87MG and U251, to achieve high silencing efficiency. The knockdown resulted in decreased cell viability in both cell lines. Transcriptome enrichment analysis of U87MG cells revealed downregulation of genes associated to tubulin acetylation, which was subsequently confirmed by Western blot analysis. Both U87MG and U251 cells exhibited downregulation of cell cycle and proliferation-related genes. Functional assays confirmed that LOXL3-knockout cells exhibited delayed cell cycle progression and significant alterations in mitotic spindles during metaphase-anaphase transition. Nuclear analysis revealed morphological changes indicative of mitotic catastrophe in U87MG cells and senescence in U251 cells. Additionally, LOXL3-knockout clones displayed reduced cell adhesion and migration. Interestingly, LOXL3 knockdown in GBM cell lines reduces tubulin acetylation, leading to mitotic catastrophe and subsequent cell death in a TP53 mutation-dependent manner. These findings highlight the potential of targeting LOXL3 as a combinatory strategy for advancing research and developing novel therapeutic approaches in TP53-mutated GBM.

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