Interplay between acute Type A aortic dissection and pan-cancer: Clinical evidence, bioinformatics, and experimental validation.

Acute Type A Aortic Dissection (ATAAD) and cancer represent major global health burdens, yet shared mechanisms remain elusive. Epidemiological analyses linked ATAAD to increased risks of lung adenocarcinoma (LUAD) and head and neck squamous cell carcinoma (HNSCC). Integrated multi-omics identified mitochondrial peptidylprolyl isomerase F (PPIF) as a key ATAAD biomarker, specifically overexpressed in monocytes, with experimentally validated. Pan-cancer analyses revealed PPIF overexpression correlated with poor prognosis across malignancies, and functional assays also confirmed PPIF drives proliferation, migration, and invasion in LUAD and HNSCC. These findings nominate PPIF as a shared mechanistic node connecting ATAAD pathogenesis to cancer progression, highlighting its potential as a therapeutic target worth further investigation.