Dataset Information


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

ABSTRACT: 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.


ORGANISM(S): Homo Sapiens

DISEASE(S): Glioblastoma

SUBMITTER: Bruno M. Costa  

PROVIDER: E-GEOD-56517 | ArrayExpress | 2015-01-30



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A transcriptomic signature mediated by HOXA9 promotes human glioblastoma initiation, aggressiveness and resistance to temozolomide.

Pojo Marta M   Gonçalves Céline S CS   Xavier-Magalhães Ana A   Oliveira Ana Isabel AI   Gonçalves Tiago T   Correia Sara S   Rodrigues Ana J AJ   Costa Sandra S   Pinto Luísa L   Pinto Afonso A AA   Lopes José M JM   Reis Rui M RM   Rocha Miguel M   Sousa Nuno N   Costa Bruno M BM  

Oncotarget 20150401 10

Glioblastoma is the most malignant brain tumor, exhibiting remarkable resistance to treatment. Here we investigated the oncogenic potential of HOXA9 in gliomagenesis, the molecular and cellular mechanisms by which HOXA9 renders glioblastoma more aggressive, and how HOXA9 affects response to chemotherapy and survival. The prognostic value of HOXA9 in glioblastoma patients was validated in two large datasets from TCGA and Rembrandt, where high HOXA9 levels were associated with shorter survival. Tr  ...[more]

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