Journal of Taibah University Medical Sciences · 2026
Metabolic effects of periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis in colorectal cancer cells.
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Gopinath Divya, Selvakumar Balachandar, Sekar Priyadharshini, Mohammed Marwan M, Li Zhengrui
Аннотация
BACKGROUND: Periodontal pathogens are increasingly recognized as key regulators of cancer biology. However, their roles in modulating metabolism-related gene expression in colorectal cancer remain poorly understood.
METHODS: Human colorectal cancer (HCT)116 cells were exposed to Fusobacterium nucleatum and Porphyromonas gingivalis for 6 h and 24 h. Expression levels of genes involved in lipid metabolism (ACAT1 and PLD2), amino acid metabolism (PAH), polyamine synthesis (SMS), kynurenine pathway (KYNU), and detoxification (ALDH2) were evaluated using quantitative real-time PCR (qPCR). The expression profiles of these genes were also compared between colorectal tumor and normal tissues using The Cancer Genome Atlas (TCGA) RNA-seq data.
RESULTS: F. nucleatum and P. gingivalis induced distinct, time-dependent metabolic changes in HCT116 cells. At 6 h, F. nucleatum upregulated KYNU, PLD2, and ACAT1 , whereas P. gingivalis broadly suppressed SMS, PAH, KYNU, ACAT1, and ALDH2. At 24 h, F. nucleatum and P. gingivalis maintained predominantly suppressive effects on KYNU, SMS, and PAH. mRNA expression analysis indicated the downregulation of ACAT1 and ALDH2, and upregulation of KYNU, PLD2, PAH, and SMS in colorectal cancer, and partial overlap with F. nucleatum-induced changes.
CONCLUSION: The distinct impacts of the two bacterial species demonstrated the complexity of colorectal cancer host-microbiome interactions. These findings suggest that microbial species may influence tumor biology through different metabolic processes, leading to diverse rather than uniform metabolic changes in colorectal cancer cells.
METHODS: Human colorectal cancer (HCT)116 cells were exposed to Fusobacterium nucleatum and Porphyromonas gingivalis for 6 h and 24 h. Expression levels of genes involved in lipid metabolism (ACAT1 and PLD2), amino acid metabolism (PAH), polyamine synthesis (SMS), kynurenine pathway (KYNU), and detoxification (ALDH2) were evaluated using quantitative real-time PCR (qPCR). The expression profiles of these genes were also compared between colorectal tumor and normal tissues using The Cancer Genome Atlas (TCGA) RNA-seq data.
RESULTS: F. nucleatum and P. gingivalis induced distinct, time-dependent metabolic changes in HCT116 cells. At 6 h, F. nucleatum upregulated KYNU, PLD2, and ACAT1 , whereas P. gingivalis broadly suppressed SMS, PAH, KYNU, ACAT1, and ALDH2. At 24 h, F. nucleatum and P. gingivalis maintained predominantly suppressive effects on KYNU, SMS, and PAH. mRNA expression analysis indicated the downregulation of ACAT1 and ALDH2, and upregulation of KYNU, PLD2, PAH, and SMS in colorectal cancer, and partial overlap with F. nucleatum-induced changes.
CONCLUSION: The distinct impacts of the two bacterial species demonstrated the complexity of colorectal cancer host-microbiome interactions. These findings suggest that microbial species may influence tumor biology through different metabolic processes, leading to diverse rather than uniform metabolic changes in colorectal cancer cells.