Evidence map›Paper›PMID 24967960›Full record

Trial reportCell death & disease2014

EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.

M Sun, X-H Liu, K-H Lu, F-Q Nie, R Xia, R Kong, J-S Yang, T-P Xu, Y-W Liu, Y-F Zou and 6 more

Open access · goldAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 8 pooled it
12.1field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 8 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Pooled it
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  9. Review
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  12. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  13. Article
  14. Review
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  16. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  17. Article
  18. Non-Coding RNAs as Key Regulators in Lung Cancer.International journal of molecular sciences · 2023
    Review
  19. Review
  20. Article

91 more citing papers are in PubMed but not listed here.

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

16 authors at 3 institutions in 1 country.

M SunDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
X-H LiuDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
K-H LuDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
F-Q NieDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
R XiaDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
R KongDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
J-S YangDepartment of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
T-P XuDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Y-W LiuDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
Y-F ZouDepartment of Obstetrics and Gynecology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
B-B LuDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
R YinDepartment of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, People's Republic of China.
E-B ZhangDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
L XuDepartment of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, People's Republic of China.
W DeDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
Z-X WangDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CNJiangsu Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence indicates that long noncoding RNAs (lncRNAs) have a critical role in the regulation of cellular processes such as differentiation, proliferation, and metastasis. These lncRNAs are dysregulated in a variety of cancers and many function as tumor suppressors; however, the regulatory factors involved in silencing lncRNA transcription are poorly understood. In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). SPRY4-IT1 is derived from an intron within SPRY4, and is upregulated in melanoma cells; knockdown of its expression leads to cell growth arrest, invasion inhibition, and elevated rates of apoptosis. Upon depletion of EZH2 by RNA interference, SPRY4-IT1 expression was restored, and transfection of SPRY4-IT1 into NSCLC cells resulted in a significant antitumoral effect, both in culture and in xenografted nude mice. Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression. In EZH2-knockdown cells, which characteristically showed impaired cell proliferation and metastasis, the induction of SPRY4-IT1 depletion partially rescued the oncogenic phenotype, suggesting that SPRY4-IT1 repression has an important role in EZH2 oncogenesis. Of most relevance, translation of these findings into human NSCLC tissue samples demonstrated that patients with low levels of SPRY4-IT1 expression had a shorter overall survival time, suggesting that SPRY4-IT1 could be a biomarker for poor prognosis of NSCLC.

Indexed as

Cell ProliferationEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsAnimalsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Line, TumorEnhancer of Zeste Homolog 2 ProteinFemaleHumansIntronsLung NeoplasmsMaleBiomarkers, TumorEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsNerve Tissue ProteinsPolycomb Repressive Complex 2RNA, Long NoncodingRNA, NeoplasmSPRY4 protein, human

Identifiers

PMID24967960
PMCPMC4611729
OpenAlexW2060430981

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.