Evidence map›Paper›PMID 31405379›Full record

ArticleClinical epigenetics2019

Aberrantly hypermethylated tumor suppressor genes were identified in oral squamous cell carcinoma (OSCC).

Soo Yeon Kim, Yu Kyeong Han, Jae Min Song, Chang Hun Lee, Keunsoo Kang, Joo Mi Yi, Hae Ryoun Park

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 73 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Soo Yeon KimDepartment of Oral Pathology, School of Dentistry, Pusan National University, Yangsan, 50612, Gyeongsangnam-do, Republic of Korea.
Yu Kyeong HanDepartment of Microbiology and Immunology, College of Medicine, Inje University, Busan, 47392, Republic of Korea.
Jae Min SongDepartment of Oral and Maxillofacial Surgery, Pusan National University, Yangsan, 50612, Gyeongsangnam-do, Republic of Korea.
Chang Hun LeeDepartment of Pathology, School of Medicine, Pusan National University, Busan, 49241, Republic of Korea.
Keunsoo KangDepartment of Microbiology, Dankook University, Cheonan, 31116, Republic of Korea.
Joo Mi YiDepartment of Microbiology and Immunology, College of Medicine, Inje University, Busan, 47392, Republic of Korea. jmyi76@inje.ac.kr.
Hae Ryoun ParkDepartment of Oral Pathology, School of Dentistry, Pusan National University, Yangsan, 50612, Gyeongsangnam-do, Republic of Korea. parkhr@pusan.ac.kr.
Pusan National University · KRInje University · KRDankook University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOral squamous cell carcinoma (OSCC) is a genetic and epigenetic disease. There is growing evidence to suggest that environmental factors due to epigenetic changes can be involved in the OSCC pathogenesis. Although tumor suppressor genes (TSGs) are commonly inactivated by promoter hypermethylation in human cancers, the epigenetic changes and the mechanism of TSGs in human OSCC remain unclear. We therefore assessed the methylation status of the TSGs, which are associated with epigenetic silencing in human cancers, OSCC cell lines, primary tumors, and normal oral mucosa.

resultsWe used 14 TSGs that were originally identified in colon cancer to investigate the aberrant hypermethylation of these genes associated with transcriptional silencing in 10 OSCC cell lines. We found three TSGs, TFPI2, SOX17, and GATA4, that are robustly hypermethylated and are associated with transcriptional silencing in OSCC cell lines. The re-expression of the three genes was induced by 5-aza-2'-deoxycytidine (5-aza-dC) in cells in which these genes were not expressed or had a lack of expression. In 33 cases of primary OSCC tumors, promoter hypermethylation was detected for the TFPI2, SOX17, and GATA4 genes at (32/33) 97%, (22/33) 67%, and (11/33) 33%, respectively. Eleven normal oral mucosa samples showed no promoter hypermethylation for all three genes, which suggests that this promoter hypermethylation is cancer-specific. Bisulfite sequencing analysis confirmed the cancer-specific methylation of the TFPI2, SOX17, and GATA4 promoters in the OSCC cell lines and tumors but not in the normal oral mucosa samples. More importantly, the methylation status of TFPI2, GATA4, and SOX17 was significantly associated with OSCC patients' overall survival through TCGA DNA methylation database.

conclusionsWe identified that TFPI2, SOX17, and GATA4 are frequently hypermethylated in human OSCC cells in a cancer-specific manner and that the transcriptional expression of these genes is regulated by promoter hypermethylation in OSCC. Our results highlight the great potential used as a synergistic biomarker set to improve the prognosis and therapeutic treatment for patients with OSCC.

Indexed as

DNA MethylationAdultAgedAged, 80 and overBiomarkers, TumorCarcinoma, Squamous CellCase-Control StudiesCell Line, TumorDown-RegulationFemaleGATA4 Transcription FactorGene Expression Regulation, NeoplasticGenes, Tumor SuppressorGlycoproteinsHumansMaleBiomarkers, TumorGATA4 protein, humanGATA4 Transcription FactorGlycoproteinsSOX17 protein, humanSOXF Transcription Factorstissue-factor-pathway inhibitor 2DNA methylationGene silencingOral squamous cell carcinomaPrognosis biomarkerTumor suppressor gene

Identifiers

PMID31405379
PMCPMC6689875
OpenAlexW2967549929

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.