Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Molecular Profiling of Breast Cancer Cells after Gemcitabine exposure

ABSTRACT: Human breast cancer cell lines were exposed to IC50 gemcitabine (Gemzar) for 24 and 48 hours. RNA was extracted, amplified and hibridized onto Oncochip microarray slides. Human breast carcinoma cell lines MCF7 and MDA-MB-231 were cultured in DMEM with Glutamax-1, supplemented with 10% fetal bovine serum, 1% penicillin-streptomycin and 0.4% fungizone. Cells were grown and passaged by trypsinization.

ORGANISM(S): Homo sapiens

SUBMITTER: Gema Moreno-Bueno

PROVIDER: E-GEOD-4937 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene expression profiling of breast cancer cells in response to gemcitabine: NF-kappaB pathway activation as a potential mechanism of resistance.

Hernández-Vargas Héctor H Rodríguez-Pinilla Socorro María SM Julián-Tendero Mercedes M Sánchez-Rovira Pedro P Cuevas Cristóbal C Antón Antonio A Ríos Maria Jesus MJ Palacios José J Moreno-Bueno Gema G

Breast cancer research and treatment 20061013 2

Gemcitabine is a nucleoside analog with clinical relevance in the treatment of several solid tumors, including breast carcinoma. In spite of its cytotoxic effect, clinical efficacy is impaired by the development of resistance. We performed gene expression analysis to shed light into the molecular mechanism of action of this drug in two breast cancer cell lines. Activation of genes related with cell cycle, cell growth and apoptosis (BNIP3L, CCNG2, DDIT4, TGFB2, TP53BP1, TP53INP1, and VEGF) was th ...[more]

PMID: 17039268

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Project description:Metaplastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticity. To advance understanding of their pathogenesis and relatedness to other breast cancer subtypes, 28 MBCs were compared with common breast cancers using comparative genomic hybridization, transcriptional profiling, and reverse-phase protein arrays and by sequencing for common breast cancer mutations. MBCs showed unique DNA copy number aberrations compared with common breast cancers. PIK3CA mutations were detected in 9 of 19 MBCs (47.4%) versus 80 of 232 hormone receptor-positive cancers (34.5%; P = 0.32), 17 of 75 HER-2-positive samples (22.7%; P = 0.04), 20 of 240 basal-like cancers (8.3%; P < 0.0001), and 0 of 14 claudin-low tumors (P = 0.004). Of 7 phosphatidylinositol 3-kinase/AKT pathway phosphorylation sites, 6 were more highly phosphorylated in MBCs than in other breast tumor subtypes. The majority of MBCs displayed mRNA profiles different from those of the most common, including basal-like cancers. By transcriptional profiling, MBCs and the recently identified claudin-low breast cancer subset constitute related receptor-negative subgroups characterized by low expression of GATA3-regulated genes and of genes responsible for cell-cell adhesion with enrichment for markers linked to stem cell function and epithelial-to-mesenchymal transition (EMT). In contrast to other breast cancers, claudin-low tumors and most MBCs showed a significant similarity to a "tumorigenic" signature defined using CD44(+)/CD24(-) breast tumor-initiating stem cell-like cells. MBCs and claudin-low tumors are thus enriched in EMT and stem cell-like features, and may arise from an earlier, more chemoresistant breast epithelial precursor than basal-like or luminal cancers. PIK3CA mutations, EMT, and stem cell-like characteristics likely contribute to the poor outcomes of MBC and suggest novel therapeutic targets. Comparison of reference samples against treatment

Dataset Information

Molecular Profiling of Breast Cancer Cells after Gemcitabine exposure

Publications

Gene expression profiling of breast cancer cells in response to gemcitabine: NF-kappaB pathway activation as a potential mechanism of resistance.

Similar Datasets

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