Evidence map›Paper›PMID 30390072›Full record

ArticleOncogene2019

Oncogenic microRNA-411 promotes lung carcinogenesis by directly targeting suppressor genes SPRY4 and TXNIP.

Caiyan Zhang, Huimin Wang, Xiaomin Liu, Yanping Hu, Lei Ding, Xing Zhang, Qiangling Sun, Yanli Li

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Role of SPRY4 in health and disease.Frontiers in oncology · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

8 authors at 3 institutions in 1 country.

Caiyan ZhangLab for Noncoding RNA and Cancer, School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Huimin WangLab for Noncoding RNA and Cancer, School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Xiaomin LiuSchool of Environmental Science and Engineering, Shanghai University, Shanghai, 200444, China.
Yanping HuLab for Noncoding RNA and Cancer, School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Lei DingLab for Noncoding RNA and Cancer, School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Xing ZhangSchool of Environmental Science and Engineering, Shanghai University, Shanghai, 200444, China.
Qiangling SunCentral Laboratory, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai, 200030, China.
Yanli LiLab for Noncoding RNA and Cancer, School of Life Sciences, Shanghai University, Shanghai, 200444, China. liyanli@shu.edu.cn.ORCID http://orcid.org/0000-0002-2936-0339
Shanghai University · CNShanghai University of Engineering Science · CNShanghai Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is one of the most common malignant diseases globally, composed of non-small cell lung cancer (NSCLC, 85%) and small cell lung cancer (SCLC, 15%). MicroRNAs (miRNAs) are single-stranded noncoding RNAs having important roles in lung cancer development. miR-411-5p/3p were reported to be increased significantly in human NSCLC tissues and cell lines. Moreover, miR-411-5p/3p overexpression could accelerate cell proliferation and migration, and impede cell apoptosis in NSCLC cell lines. Mechanically, SPRY4 is confirmed a direct target of miR-411-5p/3p. Furthermore, our findings showed that miR-411-5p/3p promoted lung tumor growth in vivo, decreased SPRY4 expression dramatically, and induced EGFR, AKT signaling activation, as well as epithelial-mesenchymal transition (EMT) simultaneously in tumor tissues. In addition, we showed that miR-411-5p also targeted tumor suppressor TXNIP, involved in regulating positively cell cycle progress in SPC-A1 cells rather than in H1299. Whether cell specificity of low TXNIP mRNA level in H1299 is responsible for the different response to cell cycle between H1299 and SPC-A1 would need further explorations. Collectively, these results suggest that miR-411-5p/3p are required for NSCLC development by suppressing SPRY4 and TXNIP; thus, the miR-411-SPRY4-AKT axis might act as a promising target for lung cancer therapy clinically.

Indexed as

A549 CellsAnimalsApoptosisCarcinogenesisCarcinoma, Non-Small-Cell LungCarrier ProteinsCell ProliferationCells, CulturedEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsCarrier ProteinsIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN411 microRNA, humanNerve Tissue ProteinsSPRY4 protein, humanTXNIP protein, human

Identifiers

PMID30390072
PMCPMC6475890
OpenAlexW2899500262

What OpenQuestion 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 OpenQuestion graph.