ArticleBioscience reports2023
Parvimonas micra infection enhances proliferation, wound healing, and inflammation of a colorectal cancer cell line.
Article in Bioscience reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Gut Microbial Dysbiosis and Male Reproductive Health: Current Insights and Future Directions.International journal of molecular sciences · 2026Review
- The microbiome in cancer.iMeta · 2025Review
- The Role of Proteomics and Genomics in the Development of Colorectal Cancer Diagnostic Tools and Potential New Treatments.ACS pharmacology & translational science · 2025Review
- Article
- The Oral Microbiome and Cancer.Advances in experimental medicine and biology · 2025Review
- Immunogenic peptides putatively from intratumor microbes: Opportunities for colorectal cancer treatment.iScience · 2024Article
- Active fraction of ground cherry (Biomedical reports · 2024Article
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- DeepPIG: deep neural network architecture with pairwise connected layers and stochastic gates using knockoff frameworks for feature selection.Scientific reports · 2024Article
- The Microbiome Matters: Its Impact on Cancer Development and Therapeutic Responses.Journal of microbiology (Seoul, Korea) · 2024Review
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gut microbiota Parvimonas micra has been found to be enriched in gut mucosal tissues and fecal samples of colorectal cancer (CRC) patients compared with non-CRC controls. In the present study, we investigated the tumorigenic potential of P. micra and its regulatory pathways in CRC using HT-29, a low-grade CRC intestinal epithelial cell. For every P. micra-HT-29 interaction assay, HT-29 was co-cultured anaerobically with P. micra at an MOI of 100:1 (bacteria: cells) for 2 h. We found that P. micra increased HT-29 cell proliferation by 38.45% (P=0.008), with the highest wound healing rate at 24 h post-infection (P=0.02). In addition, inflammatory marker expression (IL-5, IL-8, CCL20, and CSF2) was also significantly induced. Shotgun proteomics profiling analysis revealed that P. micra affects the protein expression of HT-29 (157 up-regulated and 214 down-regulated proteins). Up-regulation of PSMB4 protein and its neighbouring subunits revealed association of the ubiquitin-proteasome pathway (UPP) in CRC carcinogenesis; whereas down-regulation of CUL1, YWHAH, and MCM3 signified cell cycle dysregulation. Moreover, 22 clinically relevant epithelial-mesenchymal transition (EMT)-markers were expressed in HT-29 infected with P. micra. Overall, the present study elucidated exacerbated oncogenic properties of P. micra in HT-29 via aberrant cell proliferation, enhanced wound healing, inflammation, up-regulation of UPPs, and activation of EMT pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.