Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression in IGROV1 SP and non-SP cells


ABSTRACT: Side populations have recently been identified in ovarian cancers and may play an important role in post treatment relapse and resistance to chemotherapeutic drugs. In this study, we aimed to identify the differential expression between IGROV1 SP and NSP on Affymetrix HG-U133plus2 microarrays. We found ovarian tumour SP cells frequently over-express the multi-drug resistance associated P-glycoprotein (ABCB1) by Rank Product (FDR<0.05), and by geneset enrichment analysis, embryonic stem cell-associated ‘NOS’ signature (Notch/Oct4/Sox2 regulated genes) and Polycomb Repressive Complex 2 (PRC2) genes were over-expressed, while PRC2-repressed target genes were significantly under-expressed in the SP from ovarian cell lines compared to non-SP (FDR<10-4). Cells were isolated using Hoechst 33342 cell sorting without other treatment. The experiment was carried out in triplicates: 3 SP samples and 3 non-SP samples

ORGANISM(S): Homo sapiens

SUBMITTER: Wei Dai 

PROVIDER: E-GEOD-25191 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Ovarian cancer stem cell-like side populations are enriched following chemotherapy and overexpress EZH2.

Rizzo Siân S   Hersey Jenny M JM   Mellor Paul P   Dai Wei W   Santos-Silva Alessandra A   Liber Daniel D   Luk Louisa L   Titley Ian I   Carden Craig P CP   Box Garry G   Hudson David L DL   Kaye Stanley B SB   Brown Robert R  

Molecular cancer therapeutics 20110107 2


Platinum-based chemotherapy, with cytoreductive surgery, is the cornerstone of treatment of advanced ovarian cancer; however, acquired drug resistance is a major clinical obstacle. It has been proposed that subpopulations of tumor cells with stem cell-like properties, such as so-called side populations (SP) that overexpress ABC drug transporters, can sustain the growth of drug-resistant tumor cells, leading to tumor recurrence following chemotherapy. The histone methyltransferase EZH2 is a key c  ...[more]

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