Evidence map›Paper›PMID 41894086›Full record

ArticleMolecular biology reports2026

Porphyromonas gingivalis-derived lipopolysaccharide confers chemotherapy resistance and migratory ability on oral cancer cells by activating toll-like receptor 4 signaling pathway.

Yoshiteru Yamashita, Hideo Shigeishi, Sho Yokoyama, Ryo Uetsuki, Fumie Shiba, Shigehiro Ono, Kouji Ohta, Tomonao Aikawa

Abstract read
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Yoshiteru YamashitaDepartment of Oral and Maxillofacial Surgery, Program of Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.ORCID http://orcid.org/0009-0001-3258-5723
Hideo ShigeishiDepartment of Public Oral Health, Program of Oral Health Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734- 8553, Hiroshima, Japan. shige@hiroshima-u.ac.jp.ORCID http://orcid.org/0000-0003-0883-4299
Sho YokoyamaDepartment of Oral and Maxillofacial Surgery, Program of Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.ORCID http://orcid.org/0000-0002-9423-6609
Ryo UetsukiDepartment of Oral and Maxillofacial Surgery, Program of Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.
Fumie ShibaCollaborative Research Laboratory of Oral Inflammation Regulation, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.ORCID http://orcid.org/0000-0002-8011-5750
Shigehiro OnoDepartment of Oral and Maxillofacial Surgery, Program of Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.ORCID http://orcid.org/0000-0002-4721-2145
Kouji OhtaDepartment of Public Oral Health, Program of Oral Health Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734- 8553, Hiroshima, Japan.ORCID http://orcid.org/0000-0003-3844-1517
Tomonao AikawaDepartment of Oral and Maxillofacial Surgery, Program of Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.ORCID http://orcid.org/0000-0001-6906-6874

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study examined the Porphyromonas gingivalis-derived lipopolysaccharide (P. g-LPS)-activated-toll-like receptor 4 (TLR4) pathway and its association with resistance to chemotherapy in oral squamous cell carcinoma (OSCC) cells. METHODS AND

resultsThe OSCC cell lines OM-1 and HOC621 were used in this study. Cells were treated with P. g-LPS, TAK-242 as a TLR4 inhibitor, SC75741 as a nuclear factor-kappa B (NF-κB) inhibitor, and AH-6809 as a prostaglandin E2 (PGE2) receptor antagonist. 5-Fluorouracil (5-FU)-induced cytotoxicity was investigated by measuring lactate dehydrogenase that leaked from damaged cells. 5-FU-induced cytotoxicity was attenuated by P. g-LPS in OM-1 cells and HOC621 cells, although this attenuation was relieved by TAK-242, TLR4 siRNA knockdown, or SC75741. P. g-LPS induced phosphorylation and nuclear translocation of NF-kB/p65, and enhanced cyclooxygenase 2 (COX2) expression and PGE2 production in OM-1 cells. 5-FU-induced cytotoxicity was enhanced by AH-6809 in P. g-LPS-treated OM-1 cells. Furthermore, P. g-LPS-promoted cell migration was inhibited by TAK-242 or SC75741 in OM-1 cells. This study also involved an additional experiment focusing on CD44high OSCC cells. 5-FU-induced cytotoxicity was attenuated by P. g-LPS in amoeboid CD44high OM-1 cells when cultured on laminin-332-coated silicone gel. Additionally, P. g-LPS enhanced cofilin-1 dephosphorylation and cell protrusion in amoeboid CD44high OM-1 cells.

conclusionsP. g-LPS is involved in chemotherapy resistance of OM-1 cells by activating the TLR4/NF-kB pathway, which promotes the migratory ability of these cells, and enhancing PGE2 autocrine signaling. P. g-LPS plays a vital role in OSCC cells’ acquisition of a highly malignant phenotype.

Indexed as

Drug Resistance, NeoplasmLipopolysaccharidesMouth NeoplasmsPorphyromonas gingivalisToll-Like Receptor 4Carcinoma, Squamous CellCell Line, TumorCell MovementFluorouracilHumansNF-kappa BPhosphorylationSignal TransductionSulfonamidesToll-Like Receptor Agonistsethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateFluorouracilLipopolysaccharidesNF-kappa BSulfonamidesTLR4 protein, humanToll-Like Receptor 4Toll-Like Receptor AgonistsChemotherapy resistanceLipopolysaccharideOral squamous cell carcinomaPorphyromonas gingivalis

Identifiers

PMID41894086
PMCPMC13031245

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.