Evidence map›Paper›PMID 39589658›Full record

ArticleDiscover oncology2024

Role of early growth response-1 as a tumor suppressor in oral squamous cell carcinoma.

Yudai Shimojukkoku, Phuong Thao Nguyen, Kiyohide Ishihata, Takayuki Ishida, Yuka Kajiya, Yasunobu Oku, Koshiro Kawaguchi, Takahiro Tsuchiyama, Hideto Saijo, Kaori Shima and 1 more

Abstract read
In one paragraph

Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

11 authors.

Yudai ShimojukkokuDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Phuong Thao NguyenDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Kiyohide IshihataDepartment of Oral and Maxillofacial Surgery, Field of Oral and Maxillofacial Rehabilitation, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Takayuki IshidaDepartment of Oral and Maxillofacial Surgery, Field of Oral and Maxillofacial Rehabilitation, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Yuka KajiyaDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Yasunobu OkuDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Koshiro KawaguchiDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Takahiro TsuchiyamaDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Hideto SaijoDepartment of Oral and Maxillofacial Surgery, Field of Oral and Maxillofacial Rehabilitation, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Kaori ShimaDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan.
Tomonori SasahiraDepartment of Molecular Oral Pathology and Oncology, Field of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8544, Japan. sasa33@dent.kagoshima-u.ac.jp.

Funding

Grant-in-Aid for Scientific Research from Japan Society for the Promotion of Science 20K09912Grant-in-Aid for Scientific Research from Japan Society for the Promotion of Science 21K15401
6 · The paper itself

Abstract

backgroundOral squamous cell carcinoma (OSCC) exhibits pronounced local invasiveness and a propensity for lymph node metastasis. Given its frequent detection at advanced stages and the consequential postoperative functional impairments, the identification of effective molecular markers for early detection and treatment is imperative. Early growth response-1 (EGR-1) serves as a versatile transcription factor expressed across various cell types. Its role in cancer is contentious, acting as either an oncogene or a tumor suppressor gene.

methodsThis study undertook comprehensive analyses, including big data scrutiny, expression profiling using 50 OSCC samples, and in vitro functional assessments, to elucidate EGR-1's involvement in OSCC.

resultsComparative analysis revealed significantly reduced EGR-1 expression in oral cancer tissues compared to healthy controls or normal oral mucosa. In vitro experimentation with multiple OSCC cell lines demonstrated that EGR-1 curbed cell proliferation, migration, and invasion capabilities. Additionally, it was observed that EGR-1 prompted G0/G1 arrest in OSCC cells by modulating the activity of cell cycle regulators.

conclusionsThese findings strongly support EGR-1's tumor-suppressive role in OSCC and hint at the potential for novel OSCC therapies aimed at restoring aberrant EGR-1 function.

Indexed as

EGR1GrowthInvasionMigrationOral cancerTumor suppressor

Identifiers

PMID39589658
PMCPMC11599674

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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.