ArticleBiochemical genetics2024
Enterotoxigenic Bacteroides fragilis (ETBF) Enhances Colorectal Cancer Cell Proliferation and Metastasis Through HDAC3/miR-139-3p Pathway.
Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Guideline for designing microbiome studies in neoplastic diseases.GeroScience · 2024Guideline
- Decoding the gut microbiota-immune dialogue: from bidirectional axis to therapeutic applications.Journal of nanobiotechnology · 2026Review
- Histone deacetylases: Function in tumor development and therapeutic prospects (Review).Oncology letters · 2026Review
- Progress on the regulation of colorectal cancer and cardio-oncology by the gut microbiota and nutrients.Frontiers in immunology · 2026Review
- [Gut microbiota involved in cancer invasion and metastasis].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Article
- Primary tumor microbiomes predict distant metastasis of colorectal cancer.NPJ precision oncology · 2025Article
- Harnessing gut microbiota for colorectal cancer therapy: from clinical insights to therapeutic innovations.NPJ biofilms and microbiomes · 2025Review
- LRP11-AS1 mediates enterotoxigenic Bacteroides fragilis-related carcinogenesis in colorectal Cancer via the miR-149-3p/CDK4 pathway.Cancer gene therapy · 2025Article
- Gut microbiota - bidirectional modulator: role in inflammatory bowel disease and colorectal cancer.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Enterotoxigenic Bacteroides fragilis (ETBF) is believed to promote the malignant process of colorectal cancer (CRC), but the underlying molecular mechanism still needs to be revealed. CRC cells (SW480 and HCT-116) were treated with ETBF strain. Cell proliferation, invasion and, migration were evaluated by cell counting kit 8 assay, EdU assay, colony formation assay, transwell assay, and wound healing assay. Protein expression was analyzed by western blot. MicroRNA (miR)-139-3p and histone deacetylase 3 (HDAC3) expression levels in tissues and cells were determined by qRT-PCR. Xenograft tumor model was conducted to evaluate the effect of miR-139-3p on CRC tumor growth. ETBF treatment could promote CRC cell proliferation, invasion and migration. MiR-139-3p expression was decreased by ETBF, and its overexpression reversed the effect of ETBF on CRC cell progression. HDAC3 negatively regulated miR-139-3p expression, and its overexpression facilitated CRC cell behaviors via reducing miR-139-3p expression. Moreover, HDAC3 expression was increased by ETBF, and its knockdown also abolished ETBF-mediated CRC cell progression. Additionally, miR-139-3p overexpression could reduce CRC tumor growth in vivo. ETBF aggravated CRC proliferation and metastasis via the regulation of HDAC3/miR-139-3p axis. The discovery of ETBF/HDAC3/miR-139-3p axis may provide a new direction for CRC treatment.
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