Hirudin suppresses hematogenous metastasis by targeting desmosome junction transition in circulating tumor cell clusters via HIF-1α-DSG2 signaling.

ABSTRACT: Circulating tumor cell (CTC) clusters, key in metastasis, rely on intercellular junctions for stability. However, the specific mechanisms governing intercellular connections within CTC clusters and the strategy targeting intercellular junctions to break CTC clusters remain elusive. Anticoagulants, commonly used to manage tumor-associated thrombosis, may potentially serve as CTC cluster dissociators, but their effects and mechanisms in inhibiting tumor metastasis are unclear. Hirudin, an anticoagulant peptide was used as a tool drug and found to inhibit breast tumor lung retention and colonization through its disruption of CTC clusters rather than directly inhibiting cell migration. Further research confirmed that within CTC clusters, desmosome junctions play a dominant role in maintaining

SUBMITTER: Zou J 

PROVIDER: S-EPMC12800233 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature