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Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma [RNA-seq]

ABSTRACT: Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma [RNA-seq]

PROVIDER: PRJNA1033181 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26554615_1.fastq.gz	Fastqsanger.gz
	SRR26554615_2.fastq.gz	Fastqsanger.gz
	SRR26554616_1.fastq.gz	Fastqsanger.gz
	SRR26554616_2.fastq.gz	Fastqsanger.gz
	SRR26554617_1.fastq.gz	Fastqsanger.gz

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Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma

Project description:Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma

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Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma [scRNA-seq]

Project description:Lung adenocarcinoma (LUAD), commonly driven by KRAS mutations, is responsible for 7% of all cancer mortality. The first allele-specific KRAS inhibitors were recently approved in LUAD, but clinical benefit is limited by intrinsic and acquired resistance. LUAD predominantly arises from alveolar type 2 (AT2) cells, which function as facultative alveolar stem cells by self-renewing and replacing alveolar type 1 (AT1) cells. Using genetically engineered mouse models, patient-derived xenografts, and patient samples we found inhibition of KRAS promotes transition to a quiescent AT1-like cancer cell state in LUAD tumors. Similarly, suppressing Kras induced AT1 differentiation of wild-type AT2 cells upon lung injury. The AT1-like LUAD cells exhibited high growth and differentiation potential upon treatment cessation, whereas ablation of the AT1-like cells robustly improved treatment response to KRAS inhibitors. Our results uncover an unexpected role for KRAS in promoting intra-tumoral heterogeneity and suggest targeting alveolar differentiation may augment KRAS-targeted therapies in LUAD.

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Project description:Intra-tumoral heterogeneity in pancreatic ductal adenocarcinoma (PDAC) is characterized by a balance between basal and classical epithelial cancer cell states, with basal dominance associating with chemoresistance and a dismal prognosis. Targeting oncogenic KRAS, the primary driver of pancreatic cancer, shows early promise in clinical trials but efficacy is limited by acquired resistance. Using genetically engineered mouse models and patient-derived xenografts, we find that basal PDAC cells are highly sensitive to KRAS inhibitors. Employing fluorescent and bioluminescent reporter systems, we longitudinally track cell-state dynamics in vivo and reveal a rapid, KRAS inhibitor-induced enrichment of the classical state. Lineage-tracing identifies these enriched classical PDAC cells to be a reservoir for disease relapse. Genetic ablation of the classical cell-state is synergistic with KRAS inhibition, providing a pre-clinical proof-of-concept for this therapeutic strategy. Our findings motivate combining classical-state directed therapies with KRAS inhibitors to deepen responses and counteract resistance in pancreatic cancer.

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