SPC24 boosts tumor progression and correlates with immune infiltrates in pancreatic adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is known for its highly aggressive nature, difficult diagnosis, and resistance to treatment, resulting in a long-term five-year survival rate of less than 10%. This study focuses on the expression and function of mitotic spindle core component SPC24 in PDAC, systematically revealing its important role in tumor progression and prognosis.

Based on TCGA, GEO, and single-cell RNA sequencing data, SPC24 was significantly overexpressed in PDAC tissues and malignant cell subsets, and its expression level was significantly negatively correlated with overall survival (OS) and progression-free survival (PFS).

Bioinformatics analysis showed that SPC24-related genes were mainly enriched in cell cycle regulation, chromosome segregation and spindle assembly pathways, suggesting that SPC 24-related genes play a driving role in genomic instability and tumor clone evolution. Immunoinfiltration analysis revealed that high SPC24 expression was associated with immunosuppressive microenvironment features, such as increased M2 tumor-associated macrophages and regulatory T cells, and decreased CD8 + T cells and NK cells. Single-cell communication analysis further suggests that SPC24 may facilitate immune escape by regulating ligand-receptor interactions between tumor cells and immune cells in TME. In addition, in vitro and nude mice xenograft models verified the promotion of SPC24 on PDAC cell proliferation, migration and tumor growth. The prognostic risk model based on SPC24 showed good predictive performance and had potential clinical application value.

SPC24, as an important oncogenic factor and prognostic marker of PDAC, promotes tumor progression and treatment resistance by regulating mitotic abnormalities, metabolic reprogramming and immune microenvironment, and is worthy of being a candidate molecule for new strategies and diagnostic monitoring of targeted therapy. Future studies are needed to further explore its molecular mechanisms and potential for combination therapy to improve clinical outcomes in patients with PDAC.