Evidence map›Paper›PMID 23991831›Full record

ArticleCellular microbiology2014

Porphyromonas gingivalis promotes invasion of oral squamous cell carcinoma through induction of proMMP9 and its activation.

Hiroaki Inaba, Hideyuki Sugita, Masae Kuboniwa, Soichi Iwai, Masakazu Hamada, Takeshi Noda, Ichijiro Morisaki, Richard J Lamont, Atsuo Amano

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 4 pooled it
2.8field-weighted citation impact, top 10% 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

166 citing papers in PubMed, 4 syntheses or guidelines pooled it, 244 citations in OpenAlex.

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106 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Hiroaki InabaDepartment of Oral Frontier Biology, Center for Frontier Oral Science, Osaka University Graduate School of Dentistry, Suita, Osaka, 565-0871, Japan.
Hideyuki Sugita
Masae Kuboniwa
Soichi Iwai
Masakazu Hamada
Takeshi Noda
Ichijiro Morisaki
Richard J Lamont
Atsuo Amano
Osaka University · JPOsaka University Hospital · JPUniversity of Louisville · US

Funding

P GINGIVALIS INTERACTIONS WITH GINGIVAL EPITHELIAL CELLSR01DE011111 · NIDCR · UNIVERSITY OF WASHINGTON · PI HARIBABU BODDULURI, Richard J Lamont · 1995 to 2026
$5.4M
P.gingivalis Interactions with Gingival Epithelial CellsR37DE011111 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2009 to 2018
$3.6M
Role of JAKs in innate responses to P. gingivalisR01DE017921 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2010 to 2019
$3.3M
NIDCR NIH HHS DE11111NIDCR NIH HHS DE17921NIDCR NIH HHS R01 DE011111NIDCR NIH HHS R01 DE017921NIDCR NIH HHS R37 DE011111
6 · The paper itself

Abstract

Recent epidemiological studies have revealed a significant association between periodontitis and oral squamous cell carcinoma (OSCC). Furthermore, matrix metalloproteinase 9 (MMP9) is implicated in the invasion and metastasis of tumour cells. We examined the involvement of Porphyromonas gingivalis, a periodontal pathogen, in OSCC invasion through induced expression of proMMP and its activation. proMMP9 was continuously secreted from carcinoma SAS cells, while P. gingivalis infection increased proenzyme expression and subsequently processed it to active MMP9 in culture supernatant, which enhanced cellular invasion. In contrast, Fusobacterium nucleatum, another periodontal organism, failed to demonstrate such activities. The effects of P. gingivalis were observed with highly invasive cells, but not with the low invasivetype. P. gingivalis also stimulated proteinase-activated receptor 2 (PAR2) and enhanced proMMP9 expression, which promoted cellular invasion. P. gingivalis mutants deficient in gingipain proteases failed to activate MMP9. Infected SAS cells exhibited activation of ERK1/2, p38, and NF-kB, and their inhibitors diminished both proMMP9-overexpression and cellular invasion. Together, our results show that P. gingivalis activates the ERK1/2-Ets1, p38/HSP27, and PAR2/NF-kB pathways to induce proMMP9 expression, after which the proenzyme is activated by gingipains to promote cellular invasion of OSCC cell lines. These findings suggest a novel mechanism of progression and metastasis of OSCC associated with periodontitis.

Indexed as

Enzyme ActivationHost-Pathogen InteractionsCarcinoma, Squamous CellCell Line, TumorFusobacterium nucleatumGene ExpressionHumansMatrix Metalloproteinase 9Mouth NeoplasmsPorphyromonas gingivalisSignal TransductionTranscriptional ActivationMatrix Metalloproteinase 9

Identifiers

PMID23991831
PMCPMC3939075
OpenAlexW1909329119

What OpenQuestion holds

Textmetadata
LicenceTDM
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.