Evidence map›Paper›PMID 40244200›Full record

ArticleInternational journal of molecular sciences2025

Mechanism of Tumor Budding in Patient-Derived Metachronous Oral Primary Squamous Cell Carcinoma Cell Lines.

Takayuki Omae, Yuji Omori, Yuna Makihara, Koji Yamanegi, Soutaro Hanawa, Kyohei Yoshikawa, Kazuma Noguchi, Hiromitsu Kishimoto

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Takayuki OmaeDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.
Yuji OmoriDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.
Yuna MakiharaDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.
Koji YamanegiDepartment of Pathology, School of Medicine, Hyogo Medical University, Nishinomiya 663-8501, Japan.ORCID 0000-0002-5845-8394
Soutaro HanawaDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.
Kyohei YoshikawaDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.ORCID 0000-0002-8817-9206
Kazuma NoguchiDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.
Hiromitsu KishimotoDepartment of Oral and Maxillofacial Surgery, School of Medicine, Hyogo Medical University, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.

Funding

Grant-in-Aid for Researchers, Hyogo Medical University 210665JSPS KAKENHI 19K10277
6 · The paper itself

Abstract

Tumor budding (TB) occurs at the deepest site of tumor invasion and is a significant prognostic indicator of cervical metastasis in oral squamous cell carcinoma (OSCC). The mechanism of TB, however, remains unclear. This study investigated the roles of the tumor microenvironment and partial epithelial-mesenchymal transition (p-EMT) in TB expression using molecular and cellular physiological analyses. We established oral metachronous carcinoma cell lines (gingival carcinoma: 020, tongue carcinoma with high TB expression: 020G) from two cancers with pathologically different TB in the same patient and subjected them to exome analysis to detect gene mutations related to carcinogenesis and malignancy. Differences in EMT expression induced by transforming growth factor-β (TGF-β) between 020 and 020G were analyzed by Western blotting and reverse transcription polymerase chain reaction, and TGF-β-induced changes in cell morphology, proliferation, migration, and invasive ability were also examined. TGF-β expression was observed in the deepest tumor invasion microenvironment. TGF-β also induced the expression of several p-EMT markers and increased the migration and invasive abilities of 020G compared with 020 cells. In conclusion, TGF-β in the deep-tumor microenvironment can induce p-EMT in tumor cells, expressed as TB.

Indexed as

Carcinoma, Squamous CellMouth NeoplasmsNeoplasms, Second PrimaryCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessTransforming Growth Factor betaTumor MicroenvironmentTransforming Growth Factor betaepithelial–mesenchymal transitionmetachronous oral squamous cell carcinomatransforming growth factor-βtumor budding

Identifiers

PMID40244200
PMCPMC11989605

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Registered trials

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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.