ArticleJournal of translational medicine2023
Enterococcus faecalis promotes the progression of colorectal cancer via its metabolite: biliverdin.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 50 citations in OpenAlex.
- Beyond probiotics and pathobionts: mechanistic roles of enterococcus-derived bioactive components in health and disease.Folia microbiologica · 2026Review
- Quercetin's antitumor effect in bladder cancer: Synergistic regulation of gut microbiota and l-serine metabolic pathway.Acta pharmaceutica Sinica. B · 2026Article
- Microbiome-Shaped Metastatic Niches in Colorectal Cancer: Organ-Specific Patterns, Immune-Metabolic Mechanisms, and Therapeutic Translation.Microorganisms · 2026Review
- Gut Microbiota in Colorectal Cancer: Mechanisms of Carcinogenesis, Biomarkers, and Therapeutic Perspectives.Journal of clinical medicine · 2026Review
- Review
- Mapping of Phenotype Specific Host-Microbiome Protein-Protein Interaction Networks in Colorectal Cancer Using Deep Learning.International journal of molecular sciences · 2026Article
- Tumor-resident bacteria in gastrointestinal cancers: from regulatory mechanisms to clinical implications.Cancer biology & medicine · 2026Review
- Enterococcus faecalis-induced bystander effect causes epigenetic alterations leading to aberrant TGF-β signaling and epithelial-mesenchymal transition.Cell communication and signaling : CCS · 2026Article
- Bacterial Carbonic Anhydrase Inhibitor CAI0019 Demonstrates Efficacy inACS infectious diseases · 2026Article
- Tumor-Promoting Gut Microbes in Colorectal Cancer: Mechanisms and Translational Perspectives.International journal of medical sciences · 2026Review
- Gut microbial metabolites in colorectal cancer: dual roles in tumorigenesis, immune crosstalk, and therapeutic innovation.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Tigecycline suppresses colon cancer stem cells and impairs tumor engraftment by targeting SNAI1-regulated epithelial-mesenchymal transition.Acta pharmacologica Sinica · 2026Article
- Article
- Enterococcus-driven metabolite-host gene networks in IBD-associated colorectal carcinogenesis: integrative multi-omics and experimental validation.Frontiers in cell and developmental biology · 2026Article
- Deciphering the Post-Operative Dynamics of Opportunistic Gut Microbiota in Colorectal Cancer Patients.Microorganisms · 2025Article
- CollagenolyticSurgery open science · 2025Article
- Modulating the microbiome as an approach to anticancer drug development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fusobacterium nucleatum and non-coding RNAs: orchestrating oncogenic pathways in colorectal cancer.Gut pathogens · 2025Review
- Historical rise of cancer and dietary linoleic acid: Mechanisms and therapeutic strategies.World journal of clinical oncology · 2025Review
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEnterococcus faecalis (Efa) has been shown to be a "driver bacteria" in the occurrence and development of colorectal cancer (CRC). This study aims to explore the effect of specific metabolites of Efa on CRC.
methodsThe pro-tumor effects of Efa were assessed in colonic epithelial cells. The tumor-stimulating molecule produced by Efa was identified using liquid chromatography mass spectrometry (LC-MS). The proliferative effect of metabolites on CRC cells in vitro was assayed as well. The concentration of vascular endothelial growth factor A (VEGFA) and interleukin-8 (IL-8) was determined using enzyme-linked immunosorbent assay (ELISA). Tubular formation assay of human umbilical vein endothelial cells (HUVEC) and cell migration assay were applied to study angiogenesis. Additionally, western blot analysis was used to investigate key regulatory proteins involved in the angiogenesis pathway. Tumor growth was assessed using mouse models with two CRC cells and human colon cancer organoid.
resultsCo-incubation with the conditioned medium of Efa increased the proliferation of cultured CRC cells. Biliverdin (BV) was determined as the key metabolite produced by Efa using LC-MS screening. BV promoted colony formation and cell proliferation and inhibited cell cycle arrest of cultured CRC cells. BV significantly increased the expression level of IL-8 and VEGFA by regulating the PI3K/AKT/mTOR signaling pathway, leading to the acceleration of angiogenesis in CRC. The up-regulation of proliferation and angiogenesis by BV were also confirmed in mice.
conclusionIn conclusion, BV, as the tumor-stimulating metabolite of Efa, generates proliferative and angiogenic effects on CRC, which is mainly mediated by the activation of PI3K/AKT/mTOR.
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