Journal of Microbiology

Review

Metabolite-mediated mechanisms linking the urinary microbiome to bladder cancer: Thu Anh Trần, Ho Young Lee, Hae Woong Choi; J. Microbiol. 2025;63(11):e2509001. Published online November 30, 2025; DOI: https://doi.org/10.71150/jm.2509001

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Abstract PDF: Bladder cancer is the most common malignancy of the urinary tract and is a major health burden globally. Recent advances in microbiome research have revealed that the urinary tract harbors a resident microbial community, overturning the long-held belief in its sterility. Increasing evidence suggests that microbial dysbiosis and microbially derived metabolites contribute to bladder cancer carcinogenesis, progression, and therapeutic responses. Distinct microbial signatures have been observed in bladder cancer patients, with notable differences across disease stages and between primary and recurrent cases. Mechanistic studies have demonstrated that microbe-associated metabolites and toxins can drive DNA damage, chronic inflammation, extracellular matrix remodeling, and epithelial–mesenchymal transition. In addition, biofilm formation allows bacteria to evade immune responses and promotes persistent inflammation, creating a tumor-permissive niche. Beyond pathogenesis, microbial activity also influences therapeutic outcomes; for instance, some microbial pathways can inactivate frontline chemotherapy, while others generate metabolites with anti-tumor properties. Collectively, these patterns define a microbiota–metabolite–immunity axis, presenting opportunities for precision oncology. Targeting microbial pathways, profiling urinary microbiota, and harnessing beneficial metabolites offer promising advancements in biomarker discovery, prognostic refinement, and the development of novel therapeutic strategies for bladder cancer.

Full articles

Arctic lichen Cladonia borealis-induced cell death is mediated by p53-independent activation of Caspase-9 and PARP-1 signaling in human colorectal cancer cell lines: Ju-Mi Hong, Seul Ki Min, Kyung Hee Kim, Se Jong Han, Joung Han Yim, Sojin Kim, Youn-Jung Kim, Il-Chan Kim; J. Microbiol. 2025;63(4):e2412012. Published online April 29, 2025; DOI: https://doi.org/10.71150/jm.2412012

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Abstract PDF: The anti-cancer effects of Cladonia borealis (an Arctic lichen) methanol extract (CBME) on human colon carcinoma HCT116 cells were investigated for the first time. The proliferation of the HCT116 cells treated with CBME significantly decreased in a dose- and time-dependent manner. Flow cytometry results indicated that treatment with CBME resulted in significant apoptosis in the HCT116 cells. Furthermore, immunoblotting and qRT-PCR results revealed the expression of apoptosis-related marker genes and indicated a significant downregulation of the apoptosis regulator B-cell lymphoma expression and upregulation of the cleaved form of poly (ADP-ribose) polymerase as DNA repair and apoptosis regulators and central tumor suppressor p53. Therefore, CBME significantly inhibited cell proliferation by inducing apoptosis via the mitochondrial apoptotic pathway in colon carcinoma cells. Collectively, these data suggested that CBME contained one or more compounds with anti-cancer effects and could be a potential therapeutic agent. Further studies are required to identify candidate compounds and understand the mechanism of action of CBME.

The key pathways and genes related to oncolytic Newcastle disease virus-induced phenotypic changes in ovarian cancer cells: Wei Song, Yuan Yuan, Fangfang Cao, Huazheng Pan, Yaqing Liu; J. Microbiol. 2025;63(4):e2411018. Published online April 29, 2025; DOI: https://doi.org/10.71150/jm.2411018

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Abstract PDF Supplementary Material

The poor prognosis and high recurrence rate of ovarian cancer highlight the urgent need to develop new therapeutic strategies. Oncolytic Newcastle disease virus (NDV) can kill cancer cells directly and regulate innate and adaptive immunity. In this study, ovarian cancer cells infected with or without velogenic NDV-BJ were subjected to a CCK-8 assay for detecting cell proliferation, flow cytometry for detecting the cell cycle and apoptosis, and wound healing and transwell assays for detecting cell migration and invasion. Transcriptomic sequencing was conducted to identify the differentially expressed genes (DEGs). GO and KEGG enrichment analyses were performed to explore the mechanism underlying the oncolytic effect of NDV on ovarian cancer cells. The results showed that infection with NDV inhibited ovarian cancer cell proliferation, migration, and invasion; disrupted the cell cycle; and promoted apoptosis. Compared with those in negative control cells, the numbers of upregulated and downregulated genes in ovarian cancer cells infected with NDV were 1,499 and 2,260, respectively. Thirteen KEGG pathways related to cell growth and death, cell mobility, and signal transduction were significantly enriched. Among these pathways, 48 DEGs, especially SESN2, HLA B/C/E, GADD45B, and RELA, that may be involved in the oncolytic process were screened, and qPCR analysis verified the reliability of the transcription data. This study discovered some key pathways and genes related to oncolytic NDV-induced phenotypic changes in ovarian cancer cells, which will guide our future research directions and help further explore the specific mechanisms by which infection with NDV suppresses ovarian cancer development.

Citations

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Newcastle Disease Virus Vaccine Strain H as a Potential Oncolytic Agent in Ovarian Cancer Therapy
V. A. Sarkisova, S. Sh. Karshieva, A. A Makarova, D. O. Neymysheva, P. M. Chumakov
Molecular Biology.2025; 59(6): 1055. CrossRef

Journal Article

Upgrading Isoquercitrin Concentration via Submerge Fermentation of Mulberry Fruit Extract with Edible Probiotics to Suppress Gene Targets for Controlling Kidney Cancer and Inflammation: Md Rezaul Karim, Safia Iqbal, Shahnawaz Mohammad, Jong-Hoon Kim, Li Ling, Changbao Chen, Abdus Samad, Md Anwarul Haque, Deok-Chun Yang, Yeon Ju Kim, Dong Uk Yang; J. Microbiol. 2024;62(10):919-927. Published online October 8, 2024; DOI: https://doi.org/10.1007/s12275-024-00163-8

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