ArticleMolecular oral microbiology2010
Porphyromonas gingivalis infection sequesters pro-apoptotic Bad through Akt in primary gingival epithelial cells.
Article in Molecular oral microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.
- Association of Microbiome with Oral Squamous Cell Carcinoma: A Systematic Review of the Metagenomic Studies.International journal of environmental research and public health · 2021Pooled it
- Unraveling Oral Dysbiosis: Microbial Complexity in Common Oral Diseases.MicrobiologyOpen · 2026Review
- The Silent Link: Exploring the Impact of Periodontal Diseases on Head and Neck Carcinogenesis.Clinical and experimental dental research · 2026Review
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Microbiological Analysis Following Periodontal Treatment in Individuals with Bronchiectasis.Microorganisms · 2026Article
- Microbial crosstalk along the oral-gut axis: organ-specific oncogenic adaptations of Porphyromonas gingivalis and Fusobacterium nucleatum.Neoplasia (New York, N.Y.) · 2026Review
- Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study.BMC medical genomics · 2026Article
- A Narrative Review on Unravelling Bacterial-Mediated Carcinogenesis and Possible Alternative Treatment Strategies.BioMed research international · 2026Review
- Oral Microbiota and Carcinogenesis: Exploring the Systemic Impact of Oral Pathogens.Pathogens (Basel, Switzerland) · 2025Review
- Intestinal and esophageal microbiota in esophageal cancer development and treatment.Gut microbes · 2025Review
- Immunoinflammatory Mechanisms Connecting Periodontitis and Solid Tumors: A Systematic Review of Original Evidence.Cureus · 2025Review
- The Role ofCancers · 2025Review
- From gum inflammation to oral cancers: pyroptosis as the molecular torchbearer in periodontitis-driven carcinogenesis.Discover oncology · 2025Review
- Exploring the Oral Microbiome: Understanding its Impact on the Development of Oral Squamous Cell Carcinoma.Current microbiology · 2025Review
- Review
- Review
- Dysbiosis of Oral Microbiome: A Key Player in Oral Carcinogenesis? A Critical Review.Biomedicines · 2025Review
- Review
- Does a link exist between oral microbiota and oral squamous cell carcinoma? A review of current insights.Journal of oral microbiology · 2025Review
- Intraperitoneal Injection of theInternational journal of molecular sciences · 2024Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Porphyromonas gingivalis, a self-limiting oral pathogen, can colonize and replicate in gingival epithelial cells (GECs). P. gingivalis-infected GECs are protected from mitochondrion-dependent apoptosis, partially through activation of phosphatidyl inositol 3-kinase/Akt signaling. Biochemical events associated with P. gingivalis-induced inhibition of apoptosis include the blocking of mitochondrial membrane permeability and cytochrome-c release. We studied functional importance of Akt and the status of associated key mitochondrial molecules, pro-apoptotic Bad and caspase-9, during infection of GECs. We found that P. gingivalis infection caused significant phosphorylation of Bad progressively, while messenger RNA levels for Bad slowly decreased. Fluorescence microscopy showed translocation of the mitochondrial Bad to the cytosol post-infection. Conversely, P. gingivalis lost the ability to promote phosphorylation and translocation of Bad in Akt-deficient GECs. Caspase-9 activation induced by a chemical inducer of apoptosis was significantly inhibited by infection over time. However, Akt depletion by small interfering RNA did not reverse inhibition of caspase-9 activation by infection. Hence, P. gingivalis inactivates pro-apoptotic Bad through Akt. The inhibition of caspase-9 activation appears to be independent of Akt. Overall, our findings suggest that Akt is a key component of anti-apoptotic pathways stimulated by P. gingivalis. The P. gingivalis uses other mitochondrial pathways to protect host cells from cell-death and to ensure its survival in gingival epithelium.
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What OpenQuestion holds
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.