ArticleJournal of translational medicine2025
Colonization by Porphyromonas gingivalis in cervical squamous cell carcinomas promotes metastasis through FimA/CD151/ITGB1 signaling.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Anaerobe-Driven Inflammation and Epithelial Barrier Disruption in Genital HIV Acquisition.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Review
- Correction: Colonization by Porphyromonas gingivalis in cervical squamous cell carcinomas promotes metastasis through FimA/CD151/ITGB1 signaling.Journal of translational medicine · 2026Article
- The microbiota-host metabolic axis in cervical cancer: from homeostatic disruption to mechanisms of therapy resistance.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
19 authors.
Funding
Abstract
backgroundCervicovaginal microbiota dysbiosis has been implicated in the progression of cervical cancer. Recent studies have reported an increased abundance of Porphyromonas species in the vaginal microbiota of cervical cancer patients. Porphyromonas gingivalis (P. gingivalis), a key periodontal pathogen, has been associated with adverse pregnancy outcomes and bacterial vaginosis; however, its potential role in the progression of cervical squamous cell carcinoma (CSCC) remains largely unexplored.
methodsWe employed immunohistochemistry (IHC), 16S rRNA fluorescence in situ hybridization (FISH), and immunofluorescence to detect P. gingivalis in CSCC tissues. The association between P. gingivalis colonization and CSCC patient survival outcomes was assessed. Transwell and wound healing assays were used to assess the migration and invasion abilities of CSCC cells. In vivo xenograft mouse models were established to evaluate the impact of P. gingivalis on tumor growth and metastasis. Pull-down assays were employed to investigate interactions between the P. gingivalis fimbrial protein FimA and host cell membrane proteins. RNA sequencing and Western blotting were utilized to identify signaling pathways activated by P. gingivalis in host cells.
resultsPorphyromonas gingivalis was detected immunohistochemically in 63% of CSCC tumor tissues, with significantly higher colonization in tumors compared to adjacent nontumor tissues (P < 0.0001). The presence of P. gingivalis was significantly associated with advanced tumor stage (P < 0.01), distant metastasis (P < 0.05), lymph node metastasis (P < 0.01), and poor survival outcomes (P = 0.0257, HR = 3.167) in CSCC patients. P. gingivalis preferentially adhered to CSCC cells and promoted cell migration and invasion. In this study, animal models revealed that P. gingivalis promoted lung and lymph node metastasis in CSCC without affecting tumor growth. Pull-down assays revealed that FimA interacts with CD151 and integrin β1 (ITGB1), which are highly expressed in CSCC cells. Knockdown of CD151 and ITGB1 significantly reduced P. gingivalis adhesion to CSCC cells (P < 0.01) and suppressed its effects on cell migration and invasion (P< 0.05). P. gingivalis treatment activated the JNK/paxillin pathway and triggered actin cytoskeleton reorganization.
conclusionThis study identifies P. gingivalis as a tumor-associated bacterium that promotes CSCC metastasis through direct interaction between its fimbrial adhesin FimA and the host CD151/ITGB1 complex. This interaction activates JNK/paxillin signaling, induces cytoskeletal reorganization, and enhances the metastatic capacity of CSCC cells. Targeting this microbial-host interaction may provide a novel therapeutic intervention for P. gingivalis-driven CSCC metastasis.
Indexed as
Identifiers
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.