Expression data from MCF7 cells: control or tuberin-depleted
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Miguel Angel Pujana
PROVIDER: E-GEOD-68324 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Analysis of the expression profiles of MCF7 cells transduced with a control shRNA and an TSC2-targeted shRNA (leading to tuberin depletion).
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Project description:For this study we selected a gene, α-synuclein (SNCA), that is consistently under-expressed in MCF7 cells and breast tumors. Following transfection with an SNCA expression construct, two stable MCF7 clones (named MCF7-SNCA #1 and 2) were selected and examined for expression differences relative to the parental MCF7 cells. MCF7 cells were transfected with an expression vector containing the full-length SNCA sequence. After selection with blasticidin, two different clones were isolated and examined for expression differences relative to the parental MCF7 cells.
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Project description:Endocrine therapies targeting the proliferative effect of 17β-estradiol (17βE2) through estrogen receptor α (ERα) are the most effective systemic treatment of ERα-positive breast cancer. However, most breast tumors initially responsive to these therapies develop resistance through a molecular mechanism that is not yet fully understood. The long-term estrogen-deprived (LTED) MCF7 cell model has been proposed to recapitulate acquired resistance to aromatase inhibitors (AIs) in postmenopausal women. To elucidate this resistance, genomic, transcriptomic and molecular data were integrated into the time course of MCF7-LTED adaptation. Dynamic and widespread genomic changes were observed, including amplification of the ESR1 locus consequently linked to an increase in ERα. Dynamic transcriptomic profiles were also observed that correlated significantly with genomic changes and were influenced by transcription factors known to be involved in acquired resistance or cell proliferation (e.g. IRF1 and E2F1, respectively) but, notably, not by canonical ERα transcriptional function. Consistently, at the molecular level, activation of growth factor signaling pathways by EGFR/ERBB/AKT and a switch from phospho-Ser118 (pS118)- to pS167-ERα were observed during MCF7-LTED adaptation. Evaluation of relevant clinical settings identified significant associations between MCF7-LTED and breast tumor transcriptome profiles that characterize ERα-negative status, early response to letrozole and recurrence after tamoxifen treatment. This study proposes a mechanism for acquired resistance to estrogen deprivation that is coordinated across biological levels and independent of canonical ERα function. LTED (long term estrogen deprived) cell line was generated from MCF-7 cells by long-term culture under estrogen deprivated conditions. And RNA samples were obtained after 3, 15, 30, 90, 120, 150 and 180 days.
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Project description:Gene expression profiling was performed to identify Sfmbt1-dependent regulation in myogenic programs. To establish the magnitude of the Sfmbt1 effect on muscle cells, we have compared gene expression profiles of C2C12 cells transduced with lentiviruses expressing scramble shRNA control or shSfmbt1. Our analysis suggested that Sfmbt1 critically confers transcriptional silencing of muscle genes in myogenic progenitor cells. Two biological replicates for each sample group: C2C12 cells stably transduced with pLKO.1 expressing scramble shRNA control and C2C12 cells transduced with pLKO.1 shSFMBT1. Samples were independently cultured and RNAs were then harvested for microarray analysis.
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