Evidence map›Paper›PMID 31383552›Full record

ArticleEBioMedicine2019

MicroRNA-134 prevents the progression of esophageal squamous cell carcinoma via the PLXNA1-mediated MAPK signalling pathway.

Wei-Wei Wang, Zhi-Hua Zhao, Li Wang, Pan Li, Kui-Sheng Chen, Jian-Ying Zhang, Wen-Cai Li, Guo-Zhong Jiang, Xiang-Nan Li

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  17. PIK3C3 Acts as a Tumor Suppressor in Esophageal Squamous Cell Carcinoma and Was Regulated by MiR-340-5p.Medical science monitor : international medical journal of experimental and clinical research · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Wei-Wei WangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China.
Zhi-Hua ZhaoDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China.
Li WangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China.
Pan LiDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China.
Kui-Sheng ChenDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China.
Jian-Ying ZhangInstitute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Wen-Cai LiDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China. Electronic address: liwencai@zzu.edu.cn.
Guo-Zhong JiangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, China; Henan Key Laboratory for Tumor Pathology, Zhengzhou 450052, China. Electronic address: guozhongjiang@zzu.edu.cn.
Xiang-Nan LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. Electronic address: fcclixn@zzu.edu.cn.
First Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CNHenan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs) are involved in oncogenesis of esophageal squamous cell carcinoma (ESCC). miR-134 is reported to have a tumour-suppressive role but its role in ESCC is not known. The present study was designed to examine whether miR-134 inhibits ESCC development and further explored relevant underlying mechanisms.

methodsDifferentially expressed genes related to ESCC were identified from microarray gene expression profiles. Immunohistochemical staining and RT-qRCR assays identified elevated PLXNA1 expression levels and low miR-134. The relationship between miR-134 and PLXNA1 was predicted and further verified by a dual-luciferase reporter assay. The expression levels of miR-134 and PLXNA1 in ESCC cells were modified by miR-134 mimic/inhibitor and siRNA against PLXNA1, respectively. Thereafter, the expression of MAPK signalling pathway-related proteins, as well as the viability, migration, invasion, cell cycle and cell apoptosis of ESCC cells was investigated.

findingsThe results showed that miR-134 could block the MAPK signalling pathway by downregulating PLXNA1. When miR-134 was overexpressed or PLXNA1 was silenced, cell apoptosis was enhanced, the cell cycle was retarded, and the cell proliferation, migration and invasion were suppressed. In vivo experiments confirmed that miR-134 overexpression or PLXNA1 silencing restrained tumour growth and lymph node metastasis.

interpretationThese findings demonstrate that cancer cell proliferation, migration, invasion, and tumour metastasis of ESCC can be suppressed by overexpression of miR-134 through downregulating PLXNA1, which subsequently blocks the MAPK signalling pathway. These results provide new potential targets and strategies for the treatment of ESCC.

Indexed as

Gene Expression Regulation, NeoplasticMAP Kinase Signaling SystemAgedAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationComputational BiologyDisease ProgressionEsophageal Squamous Cell CarcinomaFemaleGene Expression ProfilingHumansImmunohistochemistryMaleMicroRNAsMIRN134 microRNA, humanNerve Tissue ProteinsPLXNA1 protein, humanReceptors, Cell SurfaceApoptosisEsophageal squamous cell carcinomaLymph node metastasisMAPK signalling pathwaymicroRNA-134PLXNA1Proliferation

Identifiers

PMID31383552
PMCPMC6711887
OpenAlexW2966136932

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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.