Evidence map›Paper›PMID 35730500›Full record

ArticleBioengineered2022

MiR-4739 inhibits the malignant behavior of esophageal squamous cell carcinoma cells via the homeobox C10/vascular endothelial growth factor A/phosphatidylinositol 3-kinase/AKT pathway.

Kaiqin Wu, Zhenchuan Liu, Chenglai Dong, Shaorui Gu, Lei Li, Wenli Wang, Yongxin Zhou

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioengineered, 2022. 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 It has been retracted, and should not be counted.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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Kaiqin WuDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Zhenchuan LiuDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Chenglai DongDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Shaorui GuDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Lei LiDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Wenli WangDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Yongxin ZhouDepartment of Thoracic-Cardiovascular Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, Jiangsu, China.
Tongji Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer is a lethal disease, and emerging evidence has shown that microRNAs are involved in its development, progression, and clinical outcome. MicroRNAs are potential biomarkers for esophageal squamous cell carcinoma (ESCC), and may be useful in advanced RNA therapy for ESCC. This study was conducted to evaluate the molecular mechanism of miR-4739 in ESCC. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to measure RNA and protein levels. Transwell assay, Cell Counting Kit-8 assay, cytometry analysis, and human umbilical vein endothelial cell tube formation assay were conducted to determine the molecular function of miR-4739 in ESCC. Potential targets of miR-4739 were predicted using bioinformatics tools and confirmed in ESCC cells using a luciferase reporter and RNA pulldown assay. Finally, we performed immunohistochemistry to evaluate the effects of administering agomir-4739 to a mouse model of ESCC. MiR-4739 expression was downregulated in ESCC tissues and cells. MiR-4739 overexpression inhibited cell proliferation, migration, and invasion, and promoted apoptosis of ESCC cells. Furthermore, vascular endothelial growth factor A expression was downregulated by miR-4739 mimics in ESCC cells. MiR-4739 negatively regulated homeobox C10 expression. Additionally, agomir-4739 inhibited tumor growth and angiogenesis

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaMicroRNAsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGenes, HomeoboxMiceNeoplasm InvasivenessPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AMicroRNAsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AAKTesophageal squamous cell carcinomahomeobox C10miR-4739therapyvascular endothelial growth factor A

Identifiers

PMID35730500
PMCPMC9342426
OpenAlexW4283271347

What OpenQuestion holds

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LicenceCC BY
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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.