Evidence map›Paper›PMID 31215741›Full record

ArticleCancer science2019

Interaction of transforming growth factor-β-Smads/microRNA-362-3p/CD82 mediated by M2 macrophages promotes the process of epithelial-mesenchymal transition in hepatocellular carcinoma cells.

Qinghui Zhang, Feng Huang, Yongliang Yao, Jianjun Wang, Jue Wei, Qiong Wu, Shihao Xiang, Ling Xu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  15. The SMAD2/miR-4256/HDAC5/p16Oncology research · 2023
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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

8 authors at 2 institutions in 1 country.

Qinghui ZhangDepartment of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University, Kunshan, China.
Feng HuangDepartment of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University, Kunshan, China.
Yongliang YaoDepartment of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University, Kunshan, China.
Jianjun WangDepartment of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University, Kunshan, China.
Jue WeiDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiong WuDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shihao XiangDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ling XuDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0002-3438-8432
Jiangsu University · CNShanghai Jiao Tong University · CN

Funding

Shanghai Changning District Municipal Science and Technology Commission, China CNKW2017Y05
6 · The paper itself

Abstract

Abnormal tumor microenvironment and the epithelial-mesenchymal transition (EMT) are important features of tumor metastasis. However, it remains unknown how signals can form complicated networks to regulate the sustainability of the EMT process. The aim of our study is to explore the possible interaction between tumor-associated macrophages and tumor cells in the EMT process mediated by microRNA (miR)-362-3p. In this study, we found that by releasing TGF-β, M2 macrophages mediate binding of Smad2/3 to miR-362-3p promoter, leading to overexpression of miR-362-3p. MicroRNA-362-3p maintains EMT by regulating CD82, one of the most important members of the family of tetraspanins. Our finding suggests that miR-362-3p can serve as a core factor mediating cross-talk between the TGF-β pathway in tumor-associated macrophages and tetraspanins in tumor cells, and thus facilitates the EMT process.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHep G2 CellsHumansKangai-1 ProteinLiver NeoplasmsMacrophagesMiceMice, NudeMicroRNAsSignal TransductionSmad2 ProteinSmad3 ProteinCD82 protein, humanKangai-1 ProteinMicroRNAsMIRN362 microRNA, humanSmad2 ProteinSmad3 ProteinTetraspaninsTransforming Growth Factor betaepithelial-mesenchymal transitionmiR-362-3pSmadTGF-βtumor-associated macrophage

Identifiers

PMID31215741
PMCPMC6676115
OpenAlexW2952189825

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.