Language

English

Publication Date

2-6-2026

Journal

Nature Communications

DOI

10.1038/s41467-026-69007-w

PMID

41651843

PMCID

PMC12881594

PubMedCentral® Posted Date

2-6-2026

PubMedCentral® Full Text Version

Post-print

Abstract

Metastatic tumor cell dissemination is the leading cause of cancer-related deaths. Clustered circulating tumor cells (CTCs) possess higher metastatic potential than single CTCs. Epithelial adherens junction (AJ) proteins typically mediate stable cell-cell interactions; however, these proteins are frequently lost in highly aggressive triple-negative breast cancers (TNBCs), raising the question of how CTCs from such tumors cluster. Here we show that the extracellular matrix (ECM) component hyaluronan (HA) mediates AJ-independent CTC clustering in TNBCs. HA is necessary and sufficient to drive clustering of tumor cells expressing its receptor CD44. Mechanistically, HA initiates contact between neighboring cells through actin-based membrane protrusions. As cells are pulled closer, these initial interactions expand to membrane-membrane contact and are subsequently stabilized by desmosomes. CTC-derived HA also acts as a docking platform to promote heterotypic cluster formation by recruiting non-CTCs, including immune cells. Thus, this ECM-receptor interaction enables CTC clustering and survival under shear stress, enhancing TNBC metastasis.

Keywords

Neoplastic Cells, Circulating, Humans, Triple Negative Breast Neoplasms, Extracellular Matrix, Female, Hyaluronic Acid, Cell Line, Tumor, Hyaluronan Receptors, Neoplasm Metastasis, Animals, Desmosomes, Adherens Junctions, Breast cancer, Metastasis, Extracellular matrix

Published Open-Access

yes

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