Evidence map›Paper›PMID 22851748›Full record

ArticleInfection and immunity2012

Enterococcus faecalis enhances cell proliferation through hydrogen peroxide-mediated epidermal growth factor receptor activation.

Kanitsak Boonanantanasarn, Ann Lindley Gill, YoonSing Yap, Vijayvel Jayaprakash, Maureen A Sullivan, Steven R Gill

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. mSphere · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Clinical, genomic, and functional characterization of vancomycin-resistantFrontiers in cellular and infection microbiology · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. The Impact ofPathogens (Basel, Switzerland) · 2024
    Review
  12. Article
  13. The role of oral microbiota in cancer.Frontiers in microbiology · 2023
    Review
  14. Review
  15. Cancer trigger or remedy: two faces of the human microbiome.Applied microbiology and biotechnology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Screening of Health-Associated Oral Bacteria for Anticancer PropertiesFrontiers in cellular and infection microbiology · 2020
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Kanitsak BoonanantanasarnDepartment of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.
Ann Lindley Gill
YoonSing Yap
Vijayvel Jayaprakash
Maureen A Sullivan
Steven R Gill
Roswell Park Comprehensive Cancer Center · USUniversity of Rochester · USMahidol University · THUniversity at Buffalo, State University of New York · US

Funding

Virology/Immunology CoreP30AI078498 · NIAID · UNIVERSITY OF ROCHESTER · PI DEWHURST, STEPHEN · 2008 to 2018
$14.6M
NIAID NIH HHS P30 AI078498
6 · The paper itself

Abstract

Enterococcus faecalis is a member of the intestinal and oral microbiota that may affect the etiology of colorectal and oral cancers. The mechanisms by which E. faecalis may contribute to the initiation and progression of these cancers remain uncertain. Epidermal growth factor receptor (EGFR) signaling is postulated to play a crucial role in oral carcinogenesis. A link between E. faecalis and EGFR signaling in oral cancer has not been elucidated. The present study aimed to evaluate the association between E. faecalis and oral cancer and to determine the underlying mechanisms that link E. faecalis to EGFR signaling. We report the high frequency of E. faecalis infection in oral tumors and the clinical association with EGFR activation. Using human oral cancer cells, we support the clinical findings and demonstrate that E. faecalis can induce EGFR activation and cell proliferation. E. faecalis activates EGFR through production of H(2)O(2), a signaling molecule that activates several signaling pathways. Inhibitors of H(2)O(2) (catalase) and EGFR (gefitinib) significantly blocked E. faecalis-induced EGFR activation and cell proliferation. Therefore, E. faecalis infection of oral tumor tissues suggests a possible association between E. faecalis infection and oral carcinogenesis. Interaction of E. faecalis with host cells and production of H(2)O(2) increase EGFR activation, thereby contributing to cell proliferation.

Indexed as

Cell ProliferationCell Line, TumorEndothelial CellsEnterococcus faecalisEnzyme-Linked Immunosorbent AssayErbB ReceptorsFemaleHumansHydrogen PeroxideMaleMiddle AgedMouth NeoplasmsSignal TransductionErbB ReceptorsHydrogen Peroxide

Identifiers

PMID22851748
PMCPMC3457582
OpenAlexW2166939001

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.