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Expression data from CHST11 over-expression in A-549 or NCI-H358 cells

ABSTRACT: Expression data from CHST11 over-expression in A-549 or NCI-H358 cells

PROVIDER: PRJNA545431 | ENA |

REPOSITORIES: ENA

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Expression data from CHST11 over-expression in A-549 or NCI-H358 cells

Project description:To examine the CHST11 controls transcriptome in NSCLC cells, we preformed the Affymetrix Human Genome U133 Plus 2.0 Array with empty vector or CHST11 expression vector in A-549 or NCI-H358 cells Then the transcriptome were compared with each other to see the CHST11-regulating gene in NSCLC cells

2022-08-31 | GSE131952 | GEO

Targeting KRAS mutant cancers with a covalent G12C-specific inhibitor

Project description:We report RNAseq gene expression data following ARS-1620 treatment and shKRAS expressing cells (NCI-H358). We also compare gene expression changes following treatment with ARS-1620 or trametinib in NCI-H358, LU65 (KRAS-G12C+), and A549 (KRAS-G12S+) cells. Additionally we report a time course (4, 24, 48hr) of ARS-1620 and trametinib treated NCI-H358 cells.

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Over-expression of YAP1 in NCI-H716 colorectal cancer cells

Project description:YAP1 plays importance roles in development of colorectal cancer as evidenced by their overexpression in colorectal cancer and their expression promoted cell proliferation and survival of colorectal cancer cells. In order to understand potential roles of YAP1 in colorectal cancer, we over-expressed constitutively active YAP1 mutant in NCI-H716 colorectal cancer cells and identified and analyzed genes whose expression is activated by YAP1 activation in colorectal cancer.

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Over-expression of YAP1 in NCI-H716 colorectal cancer cells

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Expression data from H358

Project description:Tumors that show evidence of epithelial to mesenchymal transition (EMT) have been associated with metastasis, drug resistance, and poor prognosis. EMT may alter the molecular requirements for growth and survival in different contexts, but the underlying mechanisms remain incomplete. Given the heterogeneity along the EMT spectrum between and within tumors it is important to define the requirements for growth and survival in cells with an epithelial or mesenchymal phenotype to maximize therapeutic efficacy. We have established an inducible cell line model in which a tamoxifen regulatable Twist-ER fusion protein is stably expressed in the H358 non-small cell lung cancer cell line. Upon tamoxifen addition, cells undergo EMT and provide a system in which we can compare the growth and survival requirements directly related to EMT, removing confounding factors present when comparing different cell lines. H358 cells stably expressing either GFP or TwistER were treated for 12 days in culture with 100nM 4-hydroxytamoxifen followed by RNA isolation. Three biological replicates of each condition were collected.

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Expression data from NCI-H1299 and NCI-H1299/CDDP cells

Project description:Expression data from NCI-H1299 and NCI-H1299/CDDP cells

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Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer

Project description:To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. Gene expression of H1792 cells for pre- and post-trametinib treatement was determined.

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Sinorhizobium medicae strain:549

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Rhizopus sp. 'acetoinus' strain:NRRL 549 | isolate:NRRL 549

Project description:Rhizopus acetoinus NRRL 549 Resequencing

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Comparison of gene expression in control and BRG1-knockdown H358 cell lines

Project description:Transcription was assessed in the human H358 NSCLC cell line after knockdown of BRG1, one of the mutually exclusive subunits of the SWI/SNF chromatin remodeling complex, by 2 different shRNAs.

2014-09-23 | GSE58542 | GEO

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