By integrating transcriptomic datasets and performing subsequent laboratory validation, this research sought to uncover molecular markers shared by periodontitis and colorectal cancer. Transcriptomic sequencing was performed on periodontitis and colorectal cancer tissues versus normal controls (periodontitis: n = 12 diseased vs. n = 12 healthy controls; colorectal cancer: n = 15 tumor samples vs. n = 15 matched adjacent normal tissues), using the Illumina NovaSeq 6000 platform with 150-bp paired-end sequencing. Differentially expressed genes (DEGs) underwent GO and KEGG enrichment analysis. Weighted gene co-expression network analysis (WGCNA) identified disease-associated modules. Random forest modeling and Venn analysis determined overlapping biomarkers. Experimental validation used qRT-PCR, CCK-8 viability assays, and colony formation assays in relevant cell lines. Functional analysis revealed both diseases were enriched in immune-inflammatory pathways, including cytokine signaling, TNF and NF-κB pathways. WGCNA identified distinct gene co-expression modules. Random forest analysis identified PLAC8, CLCA4, SEMA6D, CHP2, and ADAMDEC1 as top predictive features. Cross-disease analysis revealed seven shared genes. Experimental assays demonstrated a significant increase in PLAC8 and ADAMDEC1 expression, along with a marked reduction in CLCA4 under disease conditions (P < 0.001). Functional studies demonstrated that modulating these genes had a significant impact on cell viability and colony formation (P < 0.001). This study identifies shared immune-inflammatory mechanisms between periodontitis and colorectal cancer, with PLAC8, CLCA4, and ADAMDEC1 as common biomarkers, providing insights into disease linkage and potential therapeutic targets.
Peng et al. (Wed,) studied this question.