Evidence map›Paper›PMID 28963738›Full record

ArticleCell proliferation2017

Loss-of-function of miR-142 by hypermethylation promotes TGF-β-mediated tumour growth and metastasis in hepatocellular carcinoma.

Qiangfeng Yu, Leyang Xiang, Libo Yin, Xincheng Liu, Dinghua Yang, Jianyin Zhou

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. miRNAs and T cell-mediated Immune Response in Disease.The Yale journal of biology and medicine · 2025
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  16. PD-L1 and Immune Infiltration of mBioMed research international · 2021
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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 5 institutions in 1 country.

Qiangfeng YuDepartment of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou, China.
Leyang XiangDepartment of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou, China.
Libo YinDepartment of Hepatobiliary Surgery, Changzhou No. 2 People's Hospital, Nanjing Medical University, Changzhou, Jiangsu, China.
Xincheng LiuThe Second Affiliated Hospital of Shantou University Medical College, Shantou, China.
Dinghua YangDepartment of Hepatobiliary Surgery, Nanfang Hospital Affiliated to Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-4808-2186
Jianyin ZhouDepartment of Hepatobiliary and Pancreatic Surgery, Zhongshan Hospital, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0002-4396-4518
Nanfang Hospital · CNChangzhou No.2 People's Hospital · CNLongyan University · CNShantou University · CNZhongshan Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesHypermethylation-induced epigenetic silencing of tumour suppressor genes (TSGs) are frequent events during carcinogenesis. MicroRNA-142 (miR-142) is found to be dysregulated in cancer patients to participate into tumour growth, metastasis and angiogenesis. However, the tumour suppressive role of miR-142 and the status of methylation are not fully understood in hepatocellular carcinoma (HCC).

methodsHepatocellular carcinoma tissues and corresponding non-neoplastic tissues were collected. The expression and function of miR-142 and TGF-β in two HCC cell lines were determined. The miRNA-mRNA network of miR-142 was analysed in HCC cell lines.

resultsWe found that the miR-142 expression was reduced in tumour tissues and two HCC cell lines HepG2 and SMMC7721, which correlated to higher TNM stage, metastasis and differentiation. Moreover, miR-142 was identified to directly target and inhibit transforming growth factor β (TGF-β), leading to decreased cell vitality, proliferation, EMT and the ability of pro-angiogenesis in TGF-β-dependent manner. Interestingly, the status of methylation of miR-142 was analysed and the results found the hypermethylated miR-142 in tumour patients and cell lines. The treatment of methylation inhibitor 5-Aza could restore the expression of miR-142 to suppress the TGF-β expression, which impaired TGF-β-induced tumour growth.

conclusionThese findings implicated that miR-142 was a tumour suppressor gene in HCC and often hyermethylated to increase TGF-β-induced development of hepatocellular carcinoma.

Indexed as

DNA MethylationCarcinoma, HepatocellularCell Line, TumorCell ProliferationEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMicroRNAsNeoplasm MetastasisNeovascularization, PathologicTransforming Growth Factor betaMicroRNAsMIRN142 microRNA, humanTransforming Growth Factor beta

Identifiers

PMID28963738
PMCPMC6529086
OpenAlexW2757282036

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.