Evidence map›Paper›PMID 32985648›Full record

Observational studyBioscience reports2020

MiR-25-3p targets PTEN to regulate the migration, invasion, and apoptosis of esophageal cancer cells via the PI3K/AKT pathway.

Liang Zhang, Zhuang Tong, Zhe Sun, Guolian Zhu, Erdong Shen, Yanfeng Huang

RetractedAbstract readObservational StudyRetracted Publication
In one paragraph

Observational study in Bioscience reports, 2020. 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 It has been retracted, and should not be counted.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
–field-weighted citation impact
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.

  1. Article
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  7. Review
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  11. Discovery of novel mRNA demethylase FTO inhibitors against esophageal cancer.Journal of enzyme inhibition and medicinal chemistry · 2022
    Article
  12. Review
  13. Review
  14. The Relationship and Expression ofInternational journal of molecular sciences · 2022
    Article
  15. Article
  16. Article
  17. Article
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  19. Role of microRNA-25 in high glucose cultured Müller glia.International journal of ophthalmology · 2021
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Liang Zhang *Department of Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning Province 110042, China.
Zhuang Tong *Department of Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning Province 110042, China.
Zhe SunDepartment of Surgical Oncology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province 110001, China.
Guolian ZhuDepartment of Oncology, Shenyang Fifth People Hospital, Shenyang, Liaoning Province 110001, China.
Erdong ShenDepartment of Oncology, Yueyang First People's Hospital, Yueyang, Hunan 414000, China.
Yanfeng HuangDepartment of Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning Province 110042, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal cancer (EC) is one of the most common malignant tumors of the digestive system. MiR-25-3p was proved to be a biomarker for the diagnosis and treatment of many cancers. MiR-25-3p was found to be high expressed in the blood of EC patients. The aim of the present study was to explore the effect of miR-25-3p and its target gene on EC.

methodsmiR-25-3p expression in the blood of EC patients and EC cells was detected by RT-qPCR. The target of miR-25-3p was identified by bioinformatics and luciferase reporter assay. After transfection, cell viability, apoptosis, migration, and invasion were detected by MTT, flow cytometry, wound healing, and transwell assays, respectively. The expressions of PTEN, Bax, Bcl-2, cleaved Caspase-3, p-PI3K, PI3K, p-AKT, and AKT were detected by Western blot.

resultsMiR-25-3p was high expressed in the blood of EC patients and EC cells. MiR-25-3p targeted PTEN and inhibited the expression of PTEN. MiR-25-3p mimic increased the viability, migration, invasion and the expressions of Bcl-2, and inhibited the apoptosis and the expression of Bax and cleaved caspase-3 in EC cells. MiR-25-3p mimic also enhanced the expressions of p-PI3K and p-AKT and the ratios of p-PI3K/PI3K and p-AKT/AKT in EC cells. PTEN overexpression not only had an opposite effect of miR-25-3p mimic, but also reversed the effect of miR-25-3p mimic on EC cells.

conclusionMiR-25-3p targeted PTEN to promote the migration and invasion, and inhibit apoptosis of EC cells via the PI3K/AKT pathway, which might provide a new therapeutic target for EC treatment.

Indexed as

ApoptosisCase-Control StudiesCell Line, TumorCell MovementCell ProliferationEsophageal NeoplasmsGene Expression Regulation, NeoplasticHealthy VolunteersHumansMicroRNAsNeoplasm InvasivenessPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionAKT1 protein, humanMicroRNAsMIRN25 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanapoptosisesophageal cancerinvasionmigrationmiR-25-3pPTEN

Identifiers

PMID32985648
PMCPMC7560540

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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.