Urologic oncology · 2026
Microbiome-linked transcriptomic signatures in NMIBC: Toward personalized uro-oncology.
СтатьяНазвание и аннотация: Перевод в очереди
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Das Manoj, Rath Shree, Gorepatti Rohith, Dash Rishikesh, Akella Abhishek, Gaur Abhay Singh, Venugopal Giriprasad, Khan Zaiba Hasan, Ramadass Balamurugan, Nayak Prasant
Аннотация
BACKGROUND: Nonmuscle Invasive Bladder Cancer (NMIBC) is a prevalent malignancy marked by high recurrence and progression rates. Emerging evidence suggests that demographic and environmental factors may alter the bladder's native oncobiome, influencing tumor behavior. This exploratory pilot study examined whether paired tumor and adjacent normal bladder mucosa exhibit distinct host transcriptomic and microbial signatures that may illuminate early tumor-microbiome interactions in NMIBC.
METHODS: A meta-transcriptomic analysis was conducted on paired tumor and adjacent normal bladder mucosa from 6 NMIBC patients. Shotgun RNA sequencing was used to profile differential gene expression and microbial composition. Functional annotation and correlation analyses were performed to explore gene-microbe interactions.
RESULTS: Fifty-seven differentially expressed genes (DEGs) across 6 patients and 12 paired samples were identified, including 45 downregulated and 12 upregulated genes, primarily involved in extracellular matrix organization and structural integrity. Tumor tissues exhibited significantly reduced microbial species richness compared to the adjacent normal mucosa (P = 0.026). Propionibacterium acnes showed increased abundance in tumor sites (23.88%) versus the adjacent normal mucosa (13%), suggesting a protumorigenic role. Veillonella dispar and Corynebacterium durum were strongly associated with matrix-regulating genes, while Bifidobacterium longum-more abundant in the adjacent normal tissues-correlated with genes linked to extracellular homeostasis, indicating a potential protective role.
CONCLUSION: This pilot study reveals distinct transcriptomic and microbial signatures in NMIBC, highlighting the role of microbial dysbiosis, which denotes an altered microbial community; reduced diversity and shifts in key taxa relative to the adjacent bladder mucosa, in extracellular matrix remodeling and tumor progression. These host-microbe interactions may contribute to disease pathogenesis and recurrence. Further studies are warranted to elucidate the underlying mechanisms and therapeutic implications.
METHODS: A meta-transcriptomic analysis was conducted on paired tumor and adjacent normal bladder mucosa from 6 NMIBC patients. Shotgun RNA sequencing was used to profile differential gene expression and microbial composition. Functional annotation and correlation analyses were performed to explore gene-microbe interactions.
RESULTS: Fifty-seven differentially expressed genes (DEGs) across 6 patients and 12 paired samples were identified, including 45 downregulated and 12 upregulated genes, primarily involved in extracellular matrix organization and structural integrity. Tumor tissues exhibited significantly reduced microbial species richness compared to the adjacent normal mucosa (P = 0.026). Propionibacterium acnes showed increased abundance in tumor sites (23.88%) versus the adjacent normal mucosa (13%), suggesting a protumorigenic role. Veillonella dispar and Corynebacterium durum were strongly associated with matrix-regulating genes, while Bifidobacterium longum-more abundant in the adjacent normal tissues-correlated with genes linked to extracellular homeostasis, indicating a potential protective role.
CONCLUSION: This pilot study reveals distinct transcriptomic and microbial signatures in NMIBC, highlighting the role of microbial dysbiosis, which denotes an altered microbial community; reduced diversity and shifts in key taxa relative to the adjacent bladder mucosa, in extracellular matrix remodeling and tumor progression. These host-microbe interactions may contribute to disease pathogenesis and recurrence. Further studies are warranted to elucidate the underlying mechanisms and therapeutic implications.