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Id1 in mutant KRAS lung adenocarcinoma

ABSTRACT: Id1 in mutant KRAS lung adenocarcinoma

PROVIDER: PRJNA427431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6491702.fastq.gz	Fastqsanger.gz
	SRR6491703.fastq.gz	Fastqsanger.gz
	SRR6491704.fastq.gz	Fastqsanger.gz
	SRR6491705.fastq.gz	Fastqsanger.gz
	SRR6491706.fastq.gz	Fastqsanger.gz

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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

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

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

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Gene expression analysis of mouse Kras-mutant lung adenocarcinoma cells and cancer stem cells

Project description:Mechanisms underlying cancer stemness in Kras-mutant lung adenocarcinoma (KM-LUAD) are poorly understood. We previously found that mice with knockout of Gprc5a develop LUADs with somatic Kras mutations. We also previously derived Gprc5a-/- KM-LUAD cells (MDA-F471 cells) from a mouse exposed to the tobacco-specific carcinogen NNK. We also derived cancer stem cells (CSCs; grown and cultured as spheres in 3D cultures) from MDA-F471 cells. To better understand the biology of these CSCs, we compared the transcriptomes of MDA-F471 cells and their CSC counterparts by bulk RNA-sequencing.

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