Evidence map›Paper›PMID 38148658›Full record

ArticleClinical and translational medicine2023

Gender dimorphism in hepatocarcinogenesis-DNA methylation modification regulated X-chromosome inactivation escape molecule XIST.

Zhihui Dai, Sijie Wang, Xinggang Guo, Yuefan Wang, Haozan Yin, Jian Tan, Chenyang Mu, Shu-Han Sun, Hui Liu, Fu Yang

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

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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

7 citing papers in PubMed, 9 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

10 authors at 3 institutions in 1 country.

Zhihui DaiDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Sijie WangDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Xinggang GuoThird Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, China.
Yuefan WangDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Haozan YinDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Jian TanDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Chenyang MuDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Shu-Han SunDepartment of Medical Genetics, Naval Medical University, Shanghai, China.
Hui LiuThird Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, China.ORCID 0000-0003-4599-5702
Fu YangDepartment of Medical Genetics, Naval Medical University, Shanghai, China.ORCID 0000-0003-2459-3923
Second Military Medical University · CNUniversity of Shanghai for Science and Technology · CNMinistry of Education of the People's Republic of China · CN

Funding

National Key Research and Development Program of China 2016YFC1302303National Key Research and Development Program of China 2023YFC2505900National Natural Science Foundation of China 81830085National Natural Science Foundation of China 81972575National Natural Science Foundation of China 81972657
6 · The paper itself

Abstract

backgroundSex disparities constitute a significant issue in hepatocellular carcinoma (HCC). However, the mechanism of gender dimorphism in HCC is still not completely understood.

methods5-Hydroxymethylcytosine (5hmC)-Seal technology was utilised to detect the global 5hmC levels from four female and four male HCC samples. Methylation of XIST was detected by Sequenom MassARRAY methylation profiling between HCC tissues (T) and adjacent normal liver tissues (L). The role of Tet methylcytosine dioxygenase 2 (TET2) was investigated using diethylnitrosamine (DEN)-administered Tet2

resultsThe results demonstrated that the numbers of 5hmC reads in the first exon of XIST from female HCC tissues (T) were remarkably lower than that in female adjacent normal liver tissues (L). Correspondingly, DNA methylation level of XIST first exon region was significantly increased in female T than in L. By contrast, no significant change was observed in male HCC patients. Compared to L, the expression of XIST in T was also significantly downregulated. Female patients with higher XIST in HCC had a higher overall survival (OS) and more extended recurrence-free survival (RFS). Moreover, TET2 can interact with YY1 binding to the promoter region of XIST and maintain the hypomethylation state of XIST. In addition, DEN-administered Tet2

conclusionsOur study provided that YY1 and TET2 could interact to form protein complexes binding to the promoter region of XIST, regulating the methylation level of XIST and then affecting the expression of XIST. This research will provide a new clue for studying sex disparities in hepatocarcinogenesis. HIGHLIGHTS: XIST was significantly downregulated in HCC tissues and had gender disparity. Methylation levels in the XIST first exon were higher in female HCC tissues, but no significant change in male HCC patients. The TET2-YY1 complex regulate XIST expression in female hepatocytes. Other ways regulate XIST expression in male hepatocytes.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsChromosomesDNA MethylationFemaleHumansMaleMiceRNA, Long NoncodingSex CharacteristicsRNA, Long NoncodingXIST non-coding RNADNA methylationhepatocellular carcinomaTET2XIST

Identifiers

PMID38148658
PMCPMC10751514
OpenAlexW4390276654

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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.