Evidence map›Paper›PMID 30181549›Full record

ArticleOncogene2019

MYEOV functions as an amplified competing endogenous RNA in promoting metastasis by activating TGF-β pathway in NSCLC.

Lishan Fang, Shanshan Wu, Xun Zhu, Junchao Cai, Jueheng Wu, Zhenjian He, Lei Liu, Musheng Zeng, Erwei Song, Jun Li and 2 more

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

37 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. MYEOV Is a Novel Marker of Differentiated Corneal Epithelium.Investigative ophthalmology & visual science · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Evolutionarily conserved enhancer-associated features within theFrontiers in cell and developmental biology · 2024
    Article
  11. Article
  12. Article
  13. Article
  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

12 authors at 1 institution in 1 country.

Lishan FangKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Shanshan WuKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Xun ZhuKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Junchao CaiKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Jueheng WuKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Zhenjian HeSchool of Public Health, Sun Yat-sen University, Guangzhou, China.
Lei LiuKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Musheng ZengState Key Laboratory of Oncology in South China, Department of Experimental Research, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Erwei SongDepartment of Breast Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Jun LiDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Mengfeng LiKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China. limf@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-5103-6367
Hongyu GuanDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. ghongy@mail.sysu.edu.cn.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) remains a major cause of death worldwide. As metastatic disease is primarily responsible for the poor clinical outcome of NSCLC, it is important to understand the process, and its underlying molecular mechanism as well, via which NSCLC cells disseminate. In this study, we identified a new competing endogenous RNA (ceRNA), namely, the MYEOV transcript, and found that it is upregulated in NSCLC and associated with a poor prognosis of the disease. We further uncovered that the MYEOV ceRNA plays a critical role in the invasion and metastasis of NSCLC cells. Intriguingly, the MYEOV ceRNA exerted its pro-metastatic function independent of its protein-coding capacity, but in a miR-30c-2-3p binding-dependent manner. Further experiments demonstrated that the MYEOV ceRNA sequestered miR-30c-2-3p from binding its targets TGFBR2 and USP15 mRNAs, which in turn leading to constitutive activation of TGF-β signaling and tumor progression in NSCLC. By identifying a new layer of regulatory modality for TGF-β signaling, our findings extend the current understanding on the molecular mechanism mediating NSCLC progression and highlight a potential role of MYEOV transcript to serve as the therapeutic target.

Indexed as

A549 CellsAnimalsCarcinoma, Non-Small-Cell LungHumansLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm MetastasisProto-Oncogene ProteinsRNA, NeoplasmTransforming Growth Factor betaMicroRNAsMIRN30b microRNA, humanMYEOV protein, humanProto-Oncogene ProteinsRNA, NeoplasmTransforming Growth Factor beta

Identifiers

PMID30181549
PMCPMC6756124
OpenAlexW2891322638

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.