Evidence map›Paper›PMID 30718452›Full record

ArticleCell death & disease2019

miR-29c-3p regulates DNMT3B and LATS1 methylation to inhibit tumor progression in hepatocellular carcinoma.

Hao Wu, Wei Zhang, Zhenru Wu, Yan Liu, Yujun Shi, Jianping Gong, Wei Shen, Changan Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 96 citations in OpenAlex.

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6 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 1 country.

Hao WuDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Wei ZhangDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Zhenru WuLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yan LiuDepartment of Gastroenterology, The Fifth people's Hospital of Chengdu, Sichuan, 611130, China.
Yujun ShiLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, 610041, China.
Jianping GongDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Wei ShenDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. shenwei315@126.com.
Changan LiuDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. liuchangancq@163.com.
Second Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CNSichuan University · CNChengdu Fifth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests that microRNAs and DNA methylation can cause tumor suppressor gene inactivation and promote tumor malignancy. However, the functional mechanisms of miR-29c-3p and DNA methylation in hepatocellular carcinoma (HCC) are unclear. Here, we reported that miR-29c-3p expression was significantly downregulated in HCC tissues and cell lines. Low miR-29c-3p expression correlated with tumor size, multiplicity pathologic features, and shorter overall survival. Overexpression of miR-29c-3p significantly inhibited HCC cell proliferation, apoptosis, migration, and tumor growth in vivo. Moreover, DNA methyltransferases 3B (DNMT3B) was upregulated in HCC tissues, and was negatively correlated with miR-29c-3p expression. Luciferase reporter and western blotting assays revealed that DNMT3B is a target gene directly regulated by miR-29c-3p. Furthermore, miR-29c-3p regulates the methylation of large tumor suppressor gene 1 (LATS1) by DNMT3B, and abnormal methylation of LATS1 inactivates Hippo signaling pathway. We subsequently identified that high DNMT3B expression and low LATS1 expression were frequently identified in HCC tissues and were associated with poor prognosis. In conclusion, our results indicate that miR-29c-3p acts as a tumor suppressor in HCC by targeting DNMT3B and the LATS1-associated Hippo signaling pathway, which might represent a novel potential therapeutic target for HCC.

Indexed as

DNA MethylationAnimalsApoptosisCarcinoma, HepatocellularCell MovementCell ProliferationDisease ProgressionDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BDown-RegulationHep G2 CellsHeterograftsHippo Signaling PathwayHumansLiver NeoplasmsMiceDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BLATS1 protein, humanMicroRNAsMIRN29a microRNA, humanProtein Serine-Threonine Kinases

Identifiers

PMID30718452
PMCPMC6362005
OpenAlexW2912661332

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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.