Language

English

Publication Date

2-14-2023

Journal

Nature Communications

DOI

10.1038/s41467-023-36310-9

PMID

36788228

PMCID

PMC9929081

PubMedCentral® Posted Date

2-14-2023

PubMedCentral® Full Text Version

Post-Print

Abstract

Peritoneal metastasis is the leading cause of death for gastrointestinal cancers. The native and therapy-induced ascites ecosystems are not fully understood. Here, we characterize single-cell transcriptomes of 191,987 ascites cancer/immune cells from 35 patients with/without gastric cancer peritoneal metastasis (GCPM). During GCPM progression, an increase is seen of monocyte-like dendritic cells (DCs) that are pro-angiogenic with reduced antigen-presenting capacity and correlate with poor gastric cancer (GC) prognosis. We also describe the evolution of monocyte-like DCs and regulatory and proliferative T cells following therapy. Moreover, we track GC evolution, identifying high-plasticity GC clusters that exhibit a propensity to shift to a high-proliferative phenotype. Transitions occur via the recently described, autophagy-dependent plasticity program, paligenosis. Two autophagy-related genes (MARCKS and TXNIP) mark high-plasticity GC with poorer prognosis, and autophagy inhibitors induce apoptosis in patient-derived organoids. Our findings provide insights into the developmental trajectories of cancer/immune cells underlying GCPM progression and therapy resistance.

Keywords

Humans, Ascites, Peritoneal Neoplasms, Peritoneum, Stomach Neoplasms, Gastric cancer, Cancer microenvironment, Cancer microenvironment

Published Open-Access

yes

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