Evidence map›Paper›PMID 30940166›Full record

ArticleJournal of translational medicine2019

ZCCHC13-mediated induction of human liver cancer is associated with the modulation of DNA methylation and the AKT/ERK signaling pathway.

Zhiming Li, Zhi Li, Linjun Wang, Chen Long, Zaozao Zheng, Xuan Zhuang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Frontiers in cell and developmental biology · 2019
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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

6 authors at 3 institutions in 1 country.

Zhiming LiInstitute of Reproductive Health/Family Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. lzmleo@xmu.edu.cn.
Zhi LiSchool of Pharmaceutical Sciences, Xiamen University, Xiamen, 361102, Fujian, China.
Linjun WangSchool of Pharmaceutical Sciences, Xiamen University, Xiamen, 361102, Fujian, China.
Chen LongSchool of Pharmaceutical Sciences, Xiamen University, Xiamen, 361102, Fujian, China.
Zaozao ZhengSchool of Pharmaceutical Sciences, Xiamen University, Xiamen, 361102, Fujian, China.
Xuan ZhuangDepartment of Urology, The First Affiliated Hospital of Xiamen University, Xiamen, 361003, Fujian, China. zhuangxuan2006@aliyun.com.
Xiamen University · CNFirst Affiliated Hospital of Xiamen University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have shown that zinc-finger CCHC-type containing 13 (ZCCHC13) is located in an imprinted gene cluster in the X-inactivation centre, but few published studies have provided evidence of its expression in cancers. The CCHC-type zinc finger motif has numerous biological activities (such as DNA binding and RNA binding) and mediates protein-protein interactions. In an effort to examine the clinical utility of ZCCHC13 in oncology, we investigated the expression of the ZCCHC13 mRNA and protein in hepatocellular carcinoma (HCC).

methodsThe expression of the ZCCHC13 mRNA and protein was evaluated using real-time reverse transcriptase-PCR, Western blotting and immunochemistry. DNA methylation was measured by methylation-specific PCR and bisulfite sequencing. The role of ZCCHC13 methylation was further evaluated using the demethylating agent, 5-aza-2'-deoxycytidine. The presence of anti-ZCCHC13 antibodies was determined by an ELISA.

resultsZCCHC13 expression was frequently upregulated in human liver cancer cells and tissues. Compared with heathy individuals, sera from patients with HCC displayed a significant response to the recombinant ZCCHC13 protein. The overexpression of ZCCHC13 in HCC was attributed to DNA hypomethylation in the promoter region. Moreover, overexpression of ZCCHC13 in liver cancer cells promoted cell cycle progression by facilitating the G1-S transition, which was related to aberrant activation of the ATK/ERK/c-MYC/CDK pathway.

conclusionsBased on our findings, ZCCHC13 functions an oncogene for HCC, and DNA hypomethylation is a driving factor in carcinogenesis.

Indexed as

Carcinoma, HepatocellularCase-Control StudiesCell Transformation, NeoplasticDNA MethylationHeLa CellsHep G2 CellsHumansLiver NeoplasmsMAP Kinase Signaling SystemMCF-7 CellsPC-3 CellsProto-Oncogene Proteins c-aktRNA-Binding ProteinsSignal TransductionTumor Cells, CulturedProto-Oncogene Proteins c-aktRNA-Binding ProteinsZCCHC13 protein, humanDNA methylationHepatocellular carcinomaZCCHC13

Identifiers

PMID30940166
PMCPMC6444591
OpenAlexW2944145843

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.