Evidence map›Paper›PMID 30873211›Full record

ArticleCellular & molecular biology letters2019

MiR-106a directly targets LIMK1 to inhibit proliferation and EMT of oral carcinoma cells.

Bingxia Shi, Chao Ma, Guolin Liu, Yanjun Guo

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. CRISPR-Cas9-mediated gene therapy in lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. MicroRNAs as Modulators of Oral Tumorigenesis-A Focused Review.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. miR-106a Targets Anoctamin 1 (ANO1) to Regulate Lipopolysaccharide (LPS)-Induced Inflammatory Response in Macrophages.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  20. Article
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

4 authors at 1 institution in 1 country.

Bingxia Shi1Oral and Maxillofacial Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Hebei, 061000 People's Republic of China.ORCID 0000-0002-2899-7741
Chao Ma2Department of Medical Plastic Surgery, Cangzhou Central Hospital, Hebei, 061000 People's Republic of China.
Guolin Liu1Oral and Maxillofacial Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Hebei, 061000 People's Republic of China.
Yanjun Guo1Oral and Maxillofacial Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Hebei, 061000 People's Republic of China.
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLIM kinase 1 (LIMK1) expression levels are closely associated with microRNA (miRNA) processing. Higher levels of LIMK1 are reported during the progression of many cancers. Our study explored the interaction between LIMK1 and miR-106a in oral squamous cell carcinoma (OSCC).

methodsQuantitative RT-PCR was performed to detect the levels of LIMK1 and miR-106a in OSCC tissues and cell lines. The rates of cell proliferation and epithelial-mesenchymal transition (EMT) were assessed to determine the biological functions of miR-106a and LIMK1 in OSCC cells. The mRNA and protein levels of LIMK1 were measured using quantitative RT-PCR and western blotting. Luciferase assays were performed to validate LIMK1 as an miR-106a target in OSCC cells.

resultsWe found that the level of miR-106a significantly decreased and the expression of LIMK1 significantly increased in OSCC tissues and cell lines. There was a close association between these changes. Knockdown of LIMK1 significantly inhibited the proliferation and EMT of OSCC cells. The bioinformatics analysis predicted that LIMK1 is a potential target gene of miR-106a and the luciferase reporter assay confirmed that miR-106a could directly target LIMK1. Introduction of miR-106a to OSCC cells had similar effects to LIMK1 silencing. Overexpression of LIMK1 in OSCC cells partially reversed the inhibitory effects of the miR-106a mimic.

conclusionMiR-106a inhibited the cell proliferation and EMT of OSCC cells by directly decreasing LIMK1 expression.

Indexed as

Cell ProliferationEpithelial-Mesenchymal TransitionCarcinoma, Squamous CellCell Line, TumorGene Expression Regulation, NeoplasticHumansLim KinasesMicroRNAsMouth NeoplasmsLIMK1 protein, humanLim KinasesMicroRNAsMIRN106 microRNA, humanEpithelial–mesenchymal transitionLIM kinase 1MicroRNA-106aOral squamous carcinomaProliferation

Identifiers

PMID30873211
PMCPMC6402160
OpenAlexW2929311834

What Socratic holds

Textmetadata
LicenceCC BY
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.