Evidence map›Paper›PMID 29295721›Full record

ArticleOncology research2018

Downregulation of MicroRNA-135 Promotes Sensitivity of Non-Small Cell Lung Cancer to Gefitinib by Targeting TRIM16.

Ning Wang, Tingting Zhang

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 It has been retracted, and should not be counted.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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
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  6. Review
  7. LncRNA OTUD6B-AS1 overexpression promoted GPX4-mediated ferroptosis to suppress radioresistance in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  8. Review
  9. Review
  10. Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023
    Review
  11. Article
  12. Review
  13. Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Ning WangDepartment of Thoracic Surgery, Shengli Oilfield Central Hospital, Dongying, P.R. China.
Tingting ZhangDepartment of Oncology, Shengli Oilfield Central Hospital, Dongying, P.R. China.
Shengli Oilfield Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Personalized treatment targeting the epidermal growth factor receptor (EGFR) may be a promising new treatment of non-small cell lung cancer (NSCLC). Gefitinib, a tyrosine kinase inhibitor, is the first drug for NSCLC, which unfortunately easily leads to drug resistance. Our study aimed to explore the functional role of microRNA (miR)-135 in the sensitivity to gefitinib of NSCLC cells. Expression of miR-135 in normal cells and NSCLC cells was assessed, followed by the effects of abnormally expressed miR-135 on cell viability, migration, invasion, apoptosis, sensitivity to gefitinib, and the expression levels of adhesion molecules and programmed death ligand 1 (PD-L1) in H1650 and H1975 cells. Next, the possible target gene of miR-135 was screened and verified. Finally, the potential involvement of the JAK/STAT signaling pathway was investigated. Expression of miR-135 was upregulated in NSCLC cells, and miR-135 silencing repressed cell viability, migration, and invasion, but increased cell apoptosis and sensitivity to gefitinib. E-cadherin and β-catenin were significantly upregulated, but PD-L1 was downregulated by the silencing of miR-135. Subsequently, tripartite-motif (TRIM) 16 was screened and verified to be a target gene of miR-135, and miR-135 suppression was shown to function through upregulation of TRIM16 expression. Phosphorylated levels of the key kinases in the JAK/STAT pathway were reduced by silencing miR-135 by targeting TRIM16. In conclusion, miR-135 acted as a tumor promoter, and its suppression could improve sensitivity to gefitinib by targeting TRIM16 and inhibition of the JAK/STAT pathway.

Indexed as

Antineoplastic AgentsApoptosisBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationDNA-Binding ProteinsDrug Resistance, NeoplasmGefitinibGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsQuinazolinesTranscription FactorsTripartite Motif ProteinsAntineoplastic AgentsBiomarkers, TumorDNA-Binding ProteinsGefitinibMicroRNAsMIRN135 microRNA, humanQuinazolinesTranscription FactorsTRIM16 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID29295721
PMCPMC7844745
OpenAlexW2782537830

What OpenQuestion 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 OpenQuestion graph.