Evidence map›Paper›PMID 28653608›Full record

ArticleOncology research2018

MicroRNA-138 Inhibits Cell Growth, Invasion, and EMT of Non-Small Cell Lung Cancer via SOX4/p53 Feedback Loop.

Dandan Li, Changjun He, Junfeng Wang, Yanbo Wang, Jianlong Bu, Xianglong Kong, Dawei Sun

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncology research, 2018. 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 It has been retracted, and should not be counted.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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 32 citations in OpenAlex.

  1. Linc-ROR Promotes EMT by Targeting miR-204-5p/SMAD4 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Dandan LiDepartment of Pediatrics, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Changjun HeDepartment of Thoracic Surgery, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Junfeng WangDepartment of Thoracic Surgery, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Yanbo WangDepartment of Thoracic Surgery, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Jianlong BuDepartment of Thoracic Surgery, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Xianglong KongDepartment of Thoracic Surgery, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Dawei SunDepartment of Thoracic Surgery, Cancer Hospital of the Harbin Medical UniversityHarbinP.R. China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies have shown that downregulation of miR-138 occurs in a variety of cancers including non-small cell lung cancer (NSCLC). However, the precise mechanisms of miR-138 in NSCLC have not been well clarified. In this study, we investigated the biological functions and molecular mechanisms of miR-138 in NSCLC cell lines, discussing whether it could turn out to be a therapeutic biomarker of NSCLC in the future. In our study, we found that miR-138 is downregulated in NSCLC tissues and cell lines. Moreover, the low level of miR-138 was associated with increased expression of SOX4 in NSCLC tissues and cell lines. Upregulation of miR-138 significantly inhibited proliferation of NSCLC cells. In addition, invasion and EMT of NSCLC cells were suppressed by overexpression of miR-138. However, downregulation of miR-138 promoted cell growth and metastasis of NSCLC cells. Bioinformatics analysis predicted that SOX4 was a potential target gene of miR-138. Next, luciferase reporter assay confirmed that miR-138 could directly target SOX4. Consistent with the effect of miR-138, downregulation of SOX4 by siRNA inhibited proliferation, invasion, and EMT of NSCLC cells. Overexpression of SOX4 in NSCLC cells partially reversed the effect of miR-138 mimic. In addition, decreased SOX4 expression could increase the level of miR-138 via upregulation of p53. Introduction of miR-138 dramatically inhibited growth, invasion, and EMT of NSCLC cells through a SOX4/p53 feedback loop.

Indexed as

Cell ProliferationEpithelial-Mesenchymal TransitionApoptosisBiomarkers, TumorCarcinoma, Non-Small-Cell LungCase-Control StudiesCell MovementGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsNeoplasm InvasivenessPrognosisRNA, Small InterferingSOXC Transcription FactorsTumor Cells, CulturedBiomarkers, TumorMicroRNAsMIRN138 microRNA, humanRNA, Small InterferingSOX4 protein, humanSOXC Transcription FactorsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28653608
PMCPMC7844796
OpenAlexW2734101152

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.