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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

ATAC-seq of NCI-H358 cells treated with KRAS G12C inhibitor sotorasib

Project description:ATAC-seq of sotorasib-resistant NCI-H358 cells treated with sotorasib

2025-07-15 | GSE266309 | GEO

Development of acquired resistance to sotorasib in NCI-H358 cell line in vitro

Project description:NCI-H358 is a KRAS G12C-mutant non-small lung cancer cell line known to be sensitive to KRAS G12C-inhibitor sotorasib. Here, we aimed to develop sotorasib resistance in H358 and interrogate the resulting sotorasib-resistant cell line (H358-R). The H358-R cell line was created by continuous culturing of the H358 cells in sotorasib (250 nM) until cells grew readily under sotorasib pressure (approximately 2 months). We then performed RNA-seq of the resulting sotorasib-resistant cell line (H358-R) with and without sotorasib pressure, compared to the parental sensitive cell line control (H358). KRAS gene expression level was found to be increased in the sotorasib-resistant line compared with the parental cells, likely representing a mechanism of resistance. The increased KRAS expression level in the resistant cell line was maintained under sotorasib pressure.

2025-09-24 | GSE277630 | GEO

ATAC-seq of NCI-H358 cells treated with KRAS G12C inhibitor sotorasib

Project description:ATAC-seq of NCI-H358 cells treated with KRAS G12C inhibitor sotorasib

| PRJNA1106537 | ENA

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.

2015-02-04 | GSE50490 | GEO

Human kinome CRISPR knockout screen in H358 parental and sotorasib resistant H358 cells

Project description:A human kinome CRISPR knockout screen in H358 parental and sotorasib-R H358 cells using Addgene pooled libraries (#75314).

2025-10-07 | GSE275314 | 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.

2018-01-24 | GSE103021 | GEO

Effect of BRAF and MEK inhibition in KRAS mutant NSCLC cell line NCI-H358

Project description:Effect of BRAF and MEK inhibition in KRAS mutant NSCLC cell line NCI-H358

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

2015-02-04 | E-GEOD-50490 | biostudies-arrayexpress

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.

2014-01-01 | E-GEOD-52308 | biostudies-arrayexpress

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