SPI1-related protein inhibits cervical cancer cell progression and prevents macrophage cell migration.

Aim: The functions and molecular mechanisms of SPI1-related protein (SPIB) were examined in cervical cancer (CC) cells.

Methods: Genes related to miscarriage and prognosis in CC were identified by Kaplan-Meier and differential expression analysis, respectively. Cell proliferation, apoptosis, migration, and invasion were examined by cell counting kit-8, flow cytometry, transwell migration, and transwell invasion assays, respectively. The potential functions and molecular mechanisms of SPIB in CC were speculated by gene set enrichment analysis (GSEA) analysis. The mRNA and protein levels of genes were examined by RT-qPCR and western blot assays, respectively. The effect of SPIB on macrophage cells was tested by macrophage recruitment assay and bioinformatics analysis.

Results: A total of 753 dysregulated genes were identified in 88 TCGA CC samples with a history of one or more miscarriages versus 208 CC samples with no miscarriage history. Also, 91 genes related to CC prognosis were identified. SPIB, a gene related to both miscarriage and CC prognosis, inhibited Hela cell proliferation, migration, and invasion, and facilitated Hela cell apoptosis. GSEA analysis disclosed that SPIB might play vital roles in immunity, chemokine signaling pathway, and macrophage chemotaxis/activation in CC. Moreover, SPIB inhibited C-X-C motif chemokine ligand 8 (CXCL8), C-C motif chemokine ligand 17 (CCL17), and C-C motif chemokine ligand 25 (CCL25) expression in Hela cells, and SPIB overexpression in Hela cells hampered THP-1 cell migration. Higher SPIB expression was associated with less M2 macrophage infiltration in CC.

Conclusions: SPIB inhibited CC-cell progression and hindered macrophage cell migration in CC.