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Identification of miR181ab1 targets in mutant Kras lung cancer cells

ABSTRACT: Identification of miR181ab1 targets in mutant Kras lung cancer cells

PROVIDER: PRJNA527823 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8745430_1.fastq.gz	Fastqsanger.gz
	SRR8745430_2.fastq.gz	Fastqsanger.gz
	SRR8745431_1.fastq.gz	Fastqsanger.gz
	SRR8745431_2.fastq.gz	Fastqsanger.gz
	SRR8745432_1.fastq.gz	Fastqsanger.gz

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Identification of FOSL1 transcriptional targets in mutant KRAS lung adenocarcinoma cells

Project description:Identification of FOSL1 transcriptional targets in mutant KRAS lung adenocarcinoma cells

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Identification of FOSL1 transcriptional targets in mutant KRAS lung adenocarcinoma cells

Project description:Mutant KRAS lung adenocarcinoma cells, H2009, were depleted of FOSL1 by a specific shRNA and its transcriptome was profiled

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Id1 in mutant KRAS lung adenocarcinoma

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Impaired AKT signaling and lung tumorigenesis by PIERCE1 ablation in KRAS-mutant non-small cell lung cancer

Project description:KRAS-mutant non-small cell lung cancer (NSCLC) is one of the main subtypes across lung cancers. Despite the enormous studies on KRAS-mutant NSCLC, new therapeutic targets need to be identified because current therapies are insufficient. Here we show the tumor promoting function of PIERCE1 in the KRAS-mutant NSCLC. Mechanistically, PIERCE1 depletion inhibits cell growth and AKT phosphorylation (pAKT) at S473, particularly in KRAS-mutant lung cancer. Analyses of AKT-related genes show that PIERCE1 negatively regulates gene expression of AKT suppressor TRIB3 through CHOP pathway. Correspondingly, four independent in vivo approaches in lung cancer mouse models related to KRAS mutations reveal the tumor suppressive effect of PIERCE1 depletion suggesting its therapeutic potential. Tissue microarray of human lung cancer showed that PIERCE1 is expressed in 83% of lung cancers and is linked to pAKT expression. This illustrates how PIERCE1 depletion acts as a novel therapeutics against KRAS-mutant NSCLC.

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Id1 in mutant KRAS lung adenocarcinoma

Project description:Analysis of global gene expression changes in mutant KRAS lung adenocarcinoma cells upon Id1 inhibition

2020-12-14 | GSE108491 | GEO

Identification of a targetable KRAS-mutant epithelial population in non-small cell lung cancer

Project description:Lung cancer is the leading cause of cancer deaths. Tumor heterogeneity, which hampers development of targeted therapies, was herein deconvoluted via single cell RNA sequencing in aggressive human adenocarcinomas (carrying Kras-mutations) and comparable murine model. We identified a tumor-specific, mutant-KRAS-associated subpopulation which is conserved in both human and murine lung cancer. We previously reported a key role for the oncogene BMI-1 in adenocarcinomas. We therefore investigated the effects of in vivo PTC596 treatment, which affects BMI-1 activity, in our murine model. Post-treatment, MRI analysis showed decreased tumor size, while single cell transcriptomics concomitantly detected near complete ablation of the mutant-KRAS-associated subpopulation, signifying the presence of a pharmacologically targetable, tumor-associated subpopulation. Our findings therefore hold promise for the development of a targeted therapy for KRAS-mutant adenocarcinomas.

2021-09-16 | GSE136246 | GEO

Proteomics in mutant KRAS Lung cancer

Project description:Proteomic studies to check the effect of MEK1/2 and KRAS G12C inhibitors in lung cancer cells

2023-08-22 | PXD024023 | Pride

Trametinib sensitizes KRAS-mutant lung adenocarcinoma tumors to PD-1/PD-L1 axis blockade via Id1 downregulation

Project description:The identification of novel therapeutic strategies to overcome the intrinsic or acquired resistance to trametinib in mutant KRAS lung adenocarcinoma (LUAD) is a major challenge. This study analyzes the effects of trametinib in Id1, a key factor involved in the oncogenic KRAS pathway, and investigates the Id1 role in acquire resistance and synergy with immunotherapy in KRAS-driven LUAD. Restoring the antitumor immune response by blocking programmed-cell death protein 1 (PD-1) and programmed-cell death-ligand 1 (PD-L1) pathway represents a major breakthrough in non-small-cell lung cancer (NSCLC) treatment. Nevertheless, a high proportion of LUAD patients with KRAS alterations remain refractory to this therapy. Material and Methods: To explore whether MEK1/2 inhibition reduces Id1 expression, in vitro and in vivo experiments were conducted in KRAS-mutant NSCLC cells and murine models. RNAseq analysis was performed to elucidate the pathways involved in Id1 inhibition. Apoptosis and PD-L1 expression was measured by flow cytometry. Synergy of trametinib combined with anti-PD1 was investigated in KRAS-mutant LUAD mouse models. Results: Using preclinical syngeneic KRAS-mutant lung cancer mouse models, we demonstrate that trametinib synergizes with PD-1 blockade to reduce lung cancer progression and increase mice overall survival. This antitumor activity was linked to the degradation of Id1 via proteasome, and an enhanced INF-Y-mediated PD-L1 tumor cell expression in KRAS-mutant tumor cells. This effect required CD8+ T cells, boosted the intratumoral CD8+/Treg ratio, reducing the intratumoral Treg/CD4+ ratio. Conclusions: Our data may support the role of Id1 in the trametinib antitumoral effect, sustaining the mitogen-activated protein kinases (MAPK) signaling pathway involved in the trametinib acquired resistance cells and sensitizing KRAS-mutant lung tumors to PD-1 inhibitors, through PD-L1 overexpression.

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Project description:We report data on a drug combination with synergistic antitumor effect in KRAS-driven lung cancer. We used RNAseq to characterize the transcriptional changes elicited by each drug in a mutant KRAS lung cancer cell lines (H1792)

2023-08-10 | GSE161218 | GEO

cAMP response element-binding protein mediates immune-evasion of KRAS-mutant lung adenocarcinomas

Project description:We discovered that KRAS-mutant lung adenocarcinomas (LADC) co-opt CREB in order to evade the innate immune system: KRAS-driven CREB activation in LADC suppresses the expression of CXCR1 ligands that would otherwise recruit neutrophils to the tumor site. CREB was overexpressed in murine KRAS-mutant LADC, pulmonary Creb1-deletion inhibited disease development, and Creb1-overexpression boosted the tumorigenicity of KRAS-mutant cells. Conditional Creb1 deletion in Kras-mutant LADC cells caused overexpression of CXCR1/2 ligands, and lung tumor-bearing Creb1-deleted mice displayed increased pulmonary neutrophils. Cxcr1-deficient mice were selectively permissive to KRAS-mutant tumor growth and showed defective neutrophil recruitment. The pro-tumor effects of CREB required intact host-Cxcr1 and those of host-Cxcr1 necessitated mutant KRAS in cancer cells. Pharmacologic CREB blockade prevented tumor growth and restored neutrophil recruitment only when initiated before immune evasion of KRAS-mutant LADC cells. CREB and CXCR1 expression were respectively restricted to tumor and stromal cells of human LADC, while CREB-controlled genes profoundly impacted survival. In summary, CREB-mediated immune evasion of KRAS-mutant LADC rests on signaling to myeloid CXCR1 and is actionable.

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