Evidence map›Paper›PMID 31579447›Full record

ArticleIranian journal of basic medical sciences2019

MiR-96 induced non-small-cell lung cancer progression through competing endogenous RNA network and affecting EGFR signaling pathway.

Hao Ding, Mingqiang Chu, Jingjing Yue, Huaying Huang, Jian Wang, Li Zhu

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of basic medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Competing endogenous RNAs in lung cancer.Cancer biology & medicine · 2021
    Review
  3. Article
  4. 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

6 authors at 1 institution in 1 country.

Hao DingDivision of Respiratory Disease, Affiliated People's Hospital of Jiangsu University, Dianli Road No.8, Zhenjiang, 212002, China.
Mingqiang ChuDivision of Respiratory Disease, Affiliated People's Hospital of Jiangsu University, Dianli Road No.8, Zhenjiang, 212002, China.
Jingjing YueDivision of Respiratory Disease, Affiliated People's Hospital of Jiangsu University, Dianli Road No.8, Zhenjiang, 212002, China.
Huaying HuangDivision of Respiratory Disease, Affiliated People's Hospital of Jiangsu University, Dianli Road No.8, Zhenjiang, 212002, China.
Jian WangDivision of Respiratory Disease, Affiliated People's Hospital of Jiangsu University, Dianli Road No.8, Zhenjiang, 212002, China.
Li ZhuDivision of Nephrology, Affiliated People's Hospital of Jiangsu University, Dianli Road No.8, Zhenjiang, 212002, China.
Jiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesNon-small cell lung cancer (NSCLC) has become a serious global health problem in the 21st century, and tumor proliferation and metastasis are the leading causes of death in patients with lung cancer. The present study aimed to verify the function of miR-96 and miR-96 in relation to competing with endogenous RNA regulatory network in NSCLC progression including proliferation and metastasis. MATERIALS AND

methodsClinical data of miR-96 expression was collected from StarBase 2.0 developed by Sun Yat-sen University. We used wound-healing, transwell and MTT assays to measure migration, invasion and proliferation of NSCLC cell lines after different treatment. Quantitative real time PCR and western blot were used to test differential genes expression. In order to identify target between genes (FOXO1 and DUSP1) and miR-96, luciferase assay was used. Luciferase activities in FOXO1 and DUSP1 wild type plasmid groups were compared to mutant groups.

resultsqRT-PCR and online database results indicated that miR-96 is highly associated with NSCLC when compared to normal patients. In addition, miR-96 indeed induced migration, invasion and proliferation of NSCLC cell line. In addition, FOXO1 and DUSP1 are targets of miR-96 and these three molecules form competing endogenous RNA network. miR-96 related competing endogenous RNA network affects cell metastasis via epidermal growth factor receptor (EGFR) signaling.

conclusionmiR-96 can be considered as one of tumor-inducer and form competing endogenous RNA network with FOXO1 and DUSP1, which affects downstream EGFR signaling.

Indexed as

DUSP1EGFRFOXO1MetastasisMiR-96NSCLC

Identifiers

PMID31579447
PMCPMC6760481
OpenAlexW2948692150

What OpenQuestion holds

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LicenceCC BY
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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.