摘要This study explores the molecular mechanisms behind the remote transfer of thyroid cancer(THCA)by investigating the interaction network of C-X-C motif chemokine ligand 8+(CXCL8+monocytes and syndecan-1+(SDC1+)tumor stem cells using single-cell and spatial transcriptome sequencing.Tumor samples from THCA patients were analyzed using single-cell RNA sequencing(scRNA-seq),spatial transcriptome sequencing,and tumor tissue transcriptome analysis.Data were processed with Seurat and CellChat R packages,integrated via the SPOTlight package,and correlated with clinical data from the UCSC Xena database.Functional pathway enrichment analyses were performed using Gene Set Enrich-ment Analysis(GSEA),Gene Ontology(GO),and Kyoto Encyclopedia of Genes and Genome(KEGG).In vitro,a co-culture system of monocytes and THCA stem cells was developed,and protein levels were measured via enzyme-linked immunosorbent assay(ELISA)and Western blotting.The self-renewal and migration of follicular thyroid carcinoma(FTC)238-S cells were assessed through sphere formation,colony formation,Cell Counting Kit-8(CCK-8),and Transwell assays.In vivo,a subcutaneous tumor xenograft model and a lung metastasis model were established in nude mice.Transcriptomic analyses identified the CXCL8/SDC1 axis as a key mediator of Janus kinase-signal transducer and activator of transcription(JAK-STAT)signaling activation,promoting THCA stem cell self-renewal,invasion,and metastasis.CXCL8/SDC1 expression was significantly higher in the high-risk C1 subtype of THCA patients and correlated with a worse prognosis.In vitro and animal studies confirmed that the CXCL8/SDC1 axis drives tumor progression and metastasis.The interaction between CXCL8+monocytes and SDC1+tumor stem cells activates the JAK-STAT pathway,facilitating the remote transfer of THCA.Targeting the CXCL8/SDC1 axis may provide novel therapeutic strategies for improving THCA patient outcomes.