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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE266309 | GEO | 2025/07/15

REPOSITORIES: GEO

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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

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

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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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Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

Project description:Invasive mucinous adenocarcinoma (IMA) is a rare subtype of lung adenocarcinoma with a poor prognosis. Compared to non-small cell lung cancer (NSCLCs), IMA more frequently harbors KRAS mutations in the order KRAS p.G12V, p.G12D, and p.G12C. This report describes a patient with KRAS p.G12C-mutant IMA treated with sotorasib. To date, no studies have investigated the therapeutic efficacy or resistance mechanisms of sotorasib in IMA. The patient was treated with carboplatin and pemetrexed, followed by sotorasib upon disease progression. While the primary lung lesions responded well, metastatic thoracic lymph node lesions continued to increase. A pathological autopsy was performed with the family’s consent to investigate potential resistance mechanisms. RNA sequencing and additional analyses revealed increased VEGF-A expression in metastatic lymph node lesions, suggesting a role in sotorasib resistance. These findings provide insights into the molecular mechanisms underlying treatment resistance in KRAS p.G12C-mutant IMA.

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Transcriptomic characterization of sotorasib-resistant tumors in Kras-G12C/Trp53-driven LUAD in genetically engineered mice

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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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Transcriptomic changes in signaling using NCI-H358 cells treated with a KRAS G12C or a SOS1::KRASi inhibitor

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PAK and PI3K pathway activation confers resistance to KRAS<sup>G12C</sup> inhibitor sotorasib.

Project description:BackgroundKRAS is a frequently mutated oncogene in human cancer. Clinical studies on the covalent inhibitors of the KRASG12C mutant have reported promising results. However, primary and acquired resistance may limit their clinical use.MethodsSotorasib-resistant cell lines were established. We explored the signalling pathways activated in these resistant cell lines and their roles in sotorasib resistance.ResultsThe resistant cells exhibited increased cell-matrix adhesion with increased levels of stress fibres and focal adherens. p21-activated kinases (PAKs) were activated in resistant cells, which phosphorylate MEK at serine 298 of MEK and serine 338 of c-Raf to activate the mitogen-activated protein kinase pathway. The PAK inhibitors FRAX597 and FRAX486 in synergy with sotorasib reduced the viability of KRASG12C mutant cancer cells. Furthermore, the PI3K/AKT pathway was constitutively active in sotorasib-resistant cells. The overexpression of constitutively activated PI3K or the knockdown of PTEN resulted in resistance to sotorasib. PI3K inhibitor alpelisib was synergistic with sotorasib in compromising the viability of KRASG12C mutant cancer cells. Moreover, PI3K and PAK pathways formed a mutual positive regulatory loop that mediated sotorasib resistance.ConclusionsOur results indicate that the cell-matrix interaction-dependent activation of PAK mediates resistance to sotorasib through the activation of MAPK and PI3K pathways.

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Genetic changes of sotorasib-resistant cells

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