Identification of Common miRNAs Differentially Expressed in Periodontitis and Pancreatic Cancer.

Background/aim: Periodontitis is a prevalent multifactorial, oral infectious disease and is considered a high-risk factor for pancreatic cancer. Nevertheless, there is limited understanding of the underlying epigenetic mechanisms governing this relationship. The aim of this study was to identify dysregulated miRNAs associated with periodontitis and pancreatic cancer, along with their related genes, signaling pathways, and compounds.

Materials and methods: miRNA expression datasets for tissues affected by periodontitis and pancreatic cancer were obtained from the Gene Expression Omnibus database. miRNAs differentially expressed relative to normal tissues were detected, and those common to both datasets were determined. Further bioinformatics approaches were used to explore the association of common differentially expressed miRNAs with periodontitis and pancreatic cancer.

Results: Twenty shared, differentially expressed miRNAs were identified; 14 exhibited similar expression patterns in both diseases. Among these common differentially expressed miRNAs, 10 were found to be overexpressed. hsa-miR-155, hsa-miR-186, hsa-miR-765, hsa-miR-211 and hsa-miR-375 were the top miRNA nodes in the gene network, with hsa-mir-155 being the sole miRNA node in the transcription factor network. Top candidate miRNA-dysregulated genes included superoxide dismutase 2 (SOD2), nuclear FMR1 interacting protein 2 (NUFIP2), SFT2 domain-containing 2 (SFT2D2), thioredoxin-interacting protein (TXNIP), and cyclin D1 (CCND1), while top dysregulated transcription factors were Argonaute RISC catalytic component 2 (AGO2), AKT serine/threonine kinase 1 (AKT1), BCL6 transcription repressor (BCL6), breakpoint cluster region (BCR), and BRCA1 DNA repair associated (BRCA1). Relevant compounds for targeting these emerged, including 5-fluorouracil, gemcitabine, doxorubicin, ascorbate, diethylstilbestrol, and temozolomide.

Conclusion: Our study suggests candidate molecular mechanisms linking periodontitis to pancreatic cancer, highlighting potential compounds that may target both diseases. These findings provide a foundation for guiding future fundamental and clinical research.