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Papillary thyroid cancer (PTC) is the most common malignancy of the endocrine system, with an increase in incidence frequency. Major vault protein ( MVP ) is the main structural protein of the vault complex that has already been investigated in specific cancers. Yet the underlying biological functions and molecular mechanisms of  MVP  in PTC still remain considerably uncharacterized. Comprehensive analyses are predicated on several public datasets and local RNA-Seq cohort. Clinically, we found that  MVP  was upregulated in human PTC than in non-cancerous thyroid tissue and was correlated with vital clinicopathological parameters in PTC patients.  MVP  expression was associated with  BRAF  V600E ,  RAS ,  TERT , and  RET  status, and it was correlated with worse progression-free survival in PTC patients. Functionally, enrichment analysis provided new clues for the close relationship between  MVP  with cancer-related signaling pathways and the immune microenvironment in PTC. In PTC with high  MVP  expression, we found CD8 +  T cells, regulatory T cells, and follicular helper T cells have a higher infiltration level. Intriguingly,  MVP  expression was positively correlated with multiple distinct phases of the anti-cancer immunity cycle.  MVP  knockdown significantly suppressed cell viability and colony formation, and promoted apoptosis. In addition, downregulated  MVP  markedly inhibited the migration and invasion potential of PTC cells. The rescue experiments showed that  MVP  could reverse the level of cell survival and migration. Mechanistically,  MVP  exerts its oncogenic function in PTC cells through activating PI3K/AKT/mTOR and MAPK/ERK pathways. These results point out that  MVP  is a reliable biomarker related to the immune microenvironment and provide a basis for elucidating the oncogenic roles of  MVP  in PTC progression.

frontiers in cell and developmental biology

Major Vault Protein (MVP) Associated With BRAFV600E Mutation Is an Immune Microenvironment-Related Biomarker Promoting the Progression of Papillary Thyroid Cancer via MAPK/ERK and PI3K/AKT Pathways