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Blautia-PTGS1 co-occurrence in prolactinomas: potential implications for tumor microenvironment and invasiveness
Zhen Ye1,2, Jiayu Yang3, Lijin Ji4
1Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200000, China.
Context:
Prolactinomas are the most common functional pituitary adenomas. While altered gut microbiota has been observed in prolactinomas, whether these changes influence tumor behavior remains unclear. Our study integrated multi-omics data to investigate potential associations between gut microbiota composition and tumor characteristics in prolactinomas, as well as to explore potential molecular mechanisms and therapeutic pathway targets.
Methods:
Through 16S rRNA and mRNA sequencing of 10 paired patients, we identified Blautia-invasiveness associations and PTGS1 involvement in invasive heterogeneity of prolactinomas. We validated findings using large-cohort multi-omics datasets and evaluated PTGS1 as a therapeutic target in patient-derived organoids.
Results:
Blautia abundance in the gut microbiota of patients with prolactinomas correlated with tumor invasiveness. Integrating tumor transcriptomic data, we observed a positive correlation between Blautia abundance and PTGS1 expression. We leveraged previously published large-cohort multi-omics datasets and confirmed that PTGS1 is markedly upregulated in prolactinomas, with higher expression in highly invasive tumors. Differential expression analysis of tumor mRNA-seq revealed that PTGS1-high tumors showed enrichment of extracellular matrix remodeling and immune-related pathways associated with tumor invasiveness. Finally, targeting PTGS1 with the selective inhibitor Tenidap in patient-derived prolactinoma organoids suppressed organoid proliferation and prolactin secretion.
Conclusion:
We identified a correlation between Blautia abundance and PTGS1 expression in prolactinomas, with PTGS1-high tumors showing enrichment of tumor microenvironment remodeling and immune-related pathways. These findings suggest a potential Blautia-PTGS1-tumor microenvironment association in prolactinomas that requires further mechanistic investigation to establish causality. Keywords Prolactinoma, Multi-omics, Blautia, Prostaglandin endoperoxide synthase 1, Tumor environment.
