Clinicopathological Features, Immune Infiltration Landscape and Involved Signaling Pathways of the desmogleins family in Pancreatic Adenocarcinoma

Background A growing body of evidence suggests that the DSG family plays a key role in tumorigenesis and progression; however, the function of DSG family members in PAAD remains unclear. Methods Comprehensive bioinformatics analysis was performed to investigate the clinicopathological characteristics, prognostic value, imnological features, and functional mechanisms of DSG family members in PAAD, using UALCAN, the HPA, Kaplan–Meier Plotter, cBioPortal, TISIDB, LinkedOmics, STRING and GSCALite Database. Results The expression of DSG family members was significantly higher in PAAD tissues compared with paraneoplastic or normal tissues, and their copy number variation was significantly associated with poorer clinicopathological characteristics and prognosis in PAAD patients. Furthermore, the roles of DSG family members in immune regulation are diverse and complex. Mechanistically, TP53 mutations are significantly associated with promoter methylation and the expression of DSG family members, and EGFR may be key to the role of DSG family members in PAAD. DSG family members activate several oncogenic pathways, including EMT, PI3K/AKT, and RAS/MAPK signaling pathway. In addition, we found that the expression of DSG family members was significantly correlated with sensitivity to multiple conventional chemotherapeutic agents and novel targeted drugs. Conclusions DSG family members play an oncogenic role in the development of PAAD and may serve as novel biomarkers or therapeutic targets.