Colorectal cancer (CRC) is one of the most common and life-threatening malignancies worldwide. Despite extensive research, the precise molecular mechanisms underlying CRC progression remain incompletely understood. Accumulating evidence indicates that complex interactions among oncogenic signaling pathways, non-coding RNAs, and the gut microbiota play a pivotal role in CRC pathogenesis. Among oral microbiota, Porphyromonas gingivalis (P. gingivalis) has been implicated in tumorigenesis through the induction of chronic inflammation and activation of oncogenic pathways. This study aimed to investigate the expression levels of the lncRNA CCAT2 and the c-MYC, as well as to evaluate the relative abundance of P. gingivalis and Bifidobacterium bifidum (B. bifidum) in colorectal cancer tissues compared with adjacent normal tissues.

DNA and RNA were extracted from biopsy specimens obtained from 40 patients with CRC and 25 healthy controls. Complementary DNA (cDNA) was synthesized using commercial kits, and quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to measure the expression levels of CCAT2 and c-MYC, as well as the relative abundance of the 16S rRNA genes of P. gingivalis and B. bifidum.

Expression levels of lncRNA CCAT2 and c-MYC were significantly higher in CRC tissues than in normal samples (p < 0.05). Likewise, the relative abundance of P. gingivalis was significantly increased, whereas B. bifidum abundance was significantly decreased in CRC tissues (p < 0.05). In the combined study population (CRC and healthy controls), Spearman’s rank correlation analysis demonstrated significant positive correlations between P. gingivalis abundance and both CCAT2 and c-MYC expression, as well as a significant inverse correlation between B. bifidum abundance and CCAT2 expression. However, in the CRC subgroup, only the positive correlation between P. gingivalis abundance and c-MYC expression remained statistically significant.

These findings demonstrate significant associations between P. gingivalis colonization, B. bifidum depletion, and oncogenic molecular alterations in CRC. Although associations involving CCAT2 were evident in the combined cohort, only the relationship between P. gingivalis abundance and c-MYC expression persisted within the CRC subgroup, suggesting that some observed correlations may primarily reflect differences between CRC patients and healthy controls. Owing to the cross-sectional design, causal inferences cannot be drawn. Further mechanistic and longitudinal studies are warranted to validate these findings and to explore the clinical utility of microbiota-based biomarkers and therapeutic strategies.