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ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

ABSTRACT: ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

PROVIDER: PRJNA952671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24085210_1.fastq.gz	Fastqsanger.gz
	SRR24085210_2.fastq.gz	Fastqsanger.gz
	SRR24085211_1.fastq.gz	Fastqsanger.gz
	SRR24085211_2.fastq.gz	Fastqsanger.gz
	SRR24085212_1.fastq.gz	Fastqsanger.gz

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ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

Project description:ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

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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

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).

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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

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Acute and Long-Term/Resistant Gene Expression Changes in H23 Cells Due to Sotorasib Treatment

Project description:To better understand the mechanism of acquired resistance to sostorasib, we selected the H23 cells to develop an isogenic sotorasib resistant cell line. H23 cells were treated for a period of 45 days with increasing concentrations of sotorasib until the develo resistance to sostorasib.

2023-01-06 | GSE192619 | GEO

RNAseq analysis of Sotorasib sensitive and cells acquired resistance to Sotorasib

Project description:To investigate the transcriptinal alterations in Sotorasib sensitive and cells acquired resistance to Sotorasib. The Sotorasib resistant cell lines of H358 and LU65 were generated following chronic treatment with Sotorasib. We then performed gene expression profiling analysis using data obtained from RNA-seq of parental and resistant lines.

2025-10-07 | GSE275022 | GEO

ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7883

Project description:ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7884

2023-04-26 | GSE229064 | GEO

RNA-seq of HCC1576 and OVCAR8 cells treated with TEAD inhibitor GNE-7883

Project description:RNA-seq of HCC1576 and OVCAR8 cells treated with TEAD inhibitor GNE-7883

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CDK12/13 inhibition in NSCLC cell lines with acquired resistance to sotorasib

Project description:The efficacy of KRAS-G12C inhibitors in lung cancer is limited by the rapid onset of acquired resistance. While divergent mechanisms of resistance across patients and preclinical models have complicated efforts to identify therapeutic strategies for sotorasib-resistant cancers, we found that sotorasib-resistant H358 and LU65 cell lines, which have distinct mechanisms of resistance and drug sensitivity profiles, both exhibited increased vulnerability to treatment with SR-4835, an inhibitor of the transcriptional kinases CDK12 and CDK13. To identify CDK12/13-dependent genes linked to the increased sensitivity we observed in sotorasib-resistant over parental cells, we treated parental and sotorasib-resistant H358 and LU65 cells with SR-4835 and performed RNA sequencing.

2025-10-07 | GSE288707 | GEO

An allosteric pan-TEAD inhibitor blocks oncogenic YAP/TAZ signaling and overcomes KRAS G12C inhibitor resistance

Project description:The Hippo pathway is a key growth-control pathway conserved across species. The downstream effectors of the Hippo pathway YAP/TAZ are frequently activated in cancer cells by a diverse array of mechanisms to drive proliferation and survival. Based on the premise that sustained interactions between YAP/TAZ and TEADs are central to their transcriptional activities, we discovered a potent small molecule inhibitor (SMI) GNE-7883 that allosterically blocks the interactions between YAP/TAZ and all four TEAD paralogs in human cells through binding to the TEAD lipid pocket. GNE-7883 effectively reduces chromatin accessibility specifically at TEAD motifs, suppresses cell proliferation in a variety of cell line models, and achieved strong anti-tumor efficacy in vivo. Furthermore, we uncovered that GNE-7883 effectively overcomes resistance to the recently approved KRAS G12C inhibitor sotorasib in both treatment-refractory and acquired resistance cell line models, providing strong proof-of-concept of TEAD SMIs in targeting YAP/TAZ-mediated KRAS inhibitor resistance. Taken together, this work demonstrates activities of TEAD SMIs in YAP/TAZ-dependent cancers and highlights their potential broad applications in precision oncology and therapy resistance.

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