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Expression data from G9a knockdown ovarian cancer cell

ABSTRACT: G9a depleted SKCO3 cells were used to identify genes regulated by G9a-dependent epigenetic regulations We used microarrays to detail the global programme of gene expression underlying paritoneal dissemination and identified distinct classes of G9a-regulated genes during this process.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41226 | GEO | 2013/07/18

SECONDARY ACCESSION(S): PRJNA176234

REPOSITORIES: GEO

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Expression data from G9a knockdown ovarian cancer cell

Project description:G9a depleted SKCO3 cells were used to identify genes regulated by G9a-dependent epigenetic regulations We used microarrays to detail the global programme of gene expression underlying paritoneal dissemination and identified distinct classes of G9a-regulated genes during this process. SKOV3 cells receiving G9a-specific shRNAs were analyzed compare to cells receiving control shRNA

2013-07-18 | E-GEOD-41226 | biostudies-arrayexpress

Expression data from G9a overexpression and knockdown lung cancer cell lines

Project description:G9a is the major mammalian H3-K9 methyltransferase that targets euchromatic regionsand is essential for murine embryogenesis . We demonstrate that G9a is endowed with methyltransferase activity to concomitantly repress the downstream effector Ep-CAM, thereby promoting the invasion step of the invasion-metastasis cascade. We used microarrays to detail the G9a regulated gene expression underlying invasion-metastasis cascade and identified distinct classes of up-regulated genes during this process. Lung adenocarcinoma cells with G9a knockdown or overexpression were selected for RNA extraction and hybridization on Affymetrix microarrays.

2011-12-31 | E-GEOD-22810 | biostudies-arrayexpress

Expression data from G9a overexpression and knockdown lung cancer cell lines

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Expression data from Keap1 overexpression and Nrf2 knockdown lung cancer cell

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Expression data from Keap1 overexpression and Nrf2 knockdown lung cancer cell

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Expression data from knockdown of G9a in MDA-MB231 cells

2012-01-07 | GSE34925 | GEO

Expression data from knockdown of G9a in MDA-MB231 cells

Project description:G9a is an H3K9m2 methyltransferase, which is critical in controlling gene suppression and DNA methylation. We used microarray analysis to identify the target genes that are regulated by G9a in MDA-MB231 cells, in which E-cadherin is silenced. G9a expression was stably knocked-down in MDA-MB231 cells. RNA from this clone and parental (control) cells were purified for microarray analysis.

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Expression data from ovarian cancer with CHSY1 knockdown

Project description:CHSY1 has high expression in malignant tumor cells, such as colorectal cancer and ovarian cancer, and is associated with poor prognosis.The proliferation and invasion of ovarian cancer cells are weakened after knocking down CHSY1 with shRNA transfected We used microarrays to detail the global programme of gene expression underlying CHSY1 knockdown and identified distinct classes of up-regulated and down-regulated genes.

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Expression data from KSRP knockdown lung cancer cell

Project description:KSRP depleted CL1-0 cells were used to identify genes regulated by KSRP We used microarrays to detail the global programme of gene expression underlying metastasis and identified distinct classes of KSRP-regulated genes during this process.

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Change in transcriptome upon G9a knockdown in RD ERMS (Embryonal Rhabdomyosarcoma) cells

Project description:The Wnt signaling pathway is down-regulated in embryonal rhabdomyosarcoma (ERMS) and contributes to the block of myogenic differentiation. Epigenetic mechanisms leading to its suppression are unknown and could pave the way towards novel therapeutic modalities. In this study, we demonstrate that the lysine methyltransferase G9a suppresses the canonical Wnt signalling pathway by activating expression of the Wnt antagonist DKK1. Inhibition of G9a expression or activity reduced DKK1 expression and elevated canonical Wnt signalling resulting in myogenic differentiation in vitro and in vivo. Mechanistically, G9a impacted Sp1 and p300 enrichment at the DKK1 promoter in a methylation-dependent manner. The reduced tumor growth upon G9a deficiency was reversed by recombinant DKK1 or LGK974, which also inhibits Wnt signaling. Consistently, among thirteen drugs targeting chromatin modifiers, G9a inhibitors were highly effective in reducing ERMS cell viability. Together, our study demonstrates that ERMS cells are vulnerable to G9a inhibitors and suggest that targeting the G9a-DKK1--catenin node holds promise for differentiation therapy.

2020-12-16 | GSE142975 | GEO

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