Evidence map›Paper›PMID 26185536›Full record

ArticleJournal of Cancer2015

Methylation Profiling of Multiple Tumor Suppressor Genes in Hepatocellular Carcinoma and the Epigenetic Mechanism of 3OST2 Regulation.

Haiyan Chen, Tingguo Zhang, Yan Sheng, Cheng Zhang, Yunfei Peng, Xiao Wang, Cuijuan Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Signalling pathways in UHRF1-dependent regulation of tumor suppressor genes in cancer.Journal of experimental & clinical cancer research : CR · 2016
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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 1 institution in 1 country.

Haiyan Chen1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China ; 2. Department of Pathology, Shandong Provincial Chest Hospital, Jinan 250012, P. R. China.
Tingguo Zhang1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China.
Yan Sheng1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China.
Cheng Zhang1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China.
Yunfei Peng1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China.
Xiao Wang1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China.
Cuijuan Zhang1. Institute of Pathology and Pathophysiology, Shandong University School of Medicine, Jinan 250012, P. R. China.
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation is considered as a significant mechanism that silences tumor suppressor genes (TSGs) and could be used in the early diagnosis of cancer. Histone modifications often work together with DNA methylation; however, how these epigenetic alterations regulate TSGs remains unclear. Here, we determined the methylation status of ten TSGs (3OST2, ppENK, CHFR, LKB1, THBS1, HIC1, SLIT2, EDNRB, COX2, and CLDN7) in hepatocellular carcinoma (HCC) and corresponding noncancerous tissues. Methylation profiling revealed that four genes had very high frequencies of methylation in HCCs, but interestingly, similar high frequencies were also detected in corresponding noncancerous tissues (97.9% vs 95.8% for SLIT2, 93.8% vs 81.3% for EDNRB, 66.7% vs 85.4% for HIC1, and 56.3% vs 56.3% for ppENK, P > 0.05). Only the 3OST2 gene was frequently methylated in HCCs and there was significant difference between HCCs and corresponding noncancerous tissues (68.8% vs 37.5%, P < 0.05). 5-aza-2'-deoxycytidine (5-Aza-CdR) or trichostatin A (TSA) alone could partially reverse 3OST2 methylation, and their combination resulted in complete reversal. UHRF1 and histone H3R8me2s were both enriched on the hypermethylated 3OST2 promoter, but H3R8me2a was not. After 5-Aza-CdR or TSA treatment, the UHRF1 and H3R8me2s enrichment was decreased, while H3R8me2a enrichment increased. We demonstrated that 3OST2 methylation may play a critical role in the earliest steps of hepatocarcinogenesis and is directly regulated by UHRF1. Furthermore, H3R8me2s acted as a repressive mark, while H3R8me2a was correlated with 3OST2 transcriptional activity.

Indexed as

DNA methylationGene expressionHepatocellular carcinomaHistone modificationTumor suppressor gene

Identifiers

PMID26185536
PMCPMC4504110
OpenAlexW2394967773

What OpenQuestion holds

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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.