Evidence map›Paper›PMID 28831131›Full record

ArticleScientific reports2017

Nm23-H1-stabilized hnRNPA2/B1 promotes internal ribosomal entry site (IRES)-mediated translation of Sp1 in the lung cancer progression.

Chia-Yang Hung, Yi-Chang Wang, Jian-Ying Chuang, Ming-Jer Young, Hungjiun Liaw, Wen-Chang Chang, Jan-Jong Hung

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. A B1 SINE element within the mouseScience advances · 2026
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  11. BDNF-induced local translation ofScience advances · 2020
    Article
  12. The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018
    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

7 authors at 2 institutions in 1 country.

Chia-Yang HungInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yi-Chang WangInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jian-Ying ChuangThe PhD Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Ming-Jer YoungDepartment of Biotechnology and Bioindustry Science, National Cheng Kung University, Tainan, Taiwan.
Hungjiun LiawDepartment of Life Sciences, National Cheng Kung University, Tainan, Taiwan.ORCID 0000-0002-3481-709X
Wen-Chang ChangThe PhD Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Jan-Jong HungDepartment of Biotechnology and Bioindustry Science, National Cheng Kung University, Tainan, Taiwan. petehung@mail.ncku.edu.tw.
Taipei Medical University · TWNational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our recent studies have indicated that specificity protein-1 (Sp1) accumulates substantially in the early stage of lung cancer but is partially decreased in the late stages, which is an important factor in the progression of the cancer. In this study, we found that Nm23-H1 and hnRNPA2/B1 could be recruited to the 5'UTR of Sp1 mRNA. In investigating the clinical relevance of Nm23-H1/Sp1 levels, we found a positive correlation between lung cancer patients with poor prognosis and low levels of Sp1 and Nm23-H1, suggesting an association between Nm23-H1/Sp1 levels and survival rate. Knockdown of Nm23-H1 inhibits lung cancer growth but increases lung cancer cell malignancy, which could be rescued by overexpression of Sp1, indicating that Nm23-H1-induced Sp1 expression is critical for lung cancer progression. We also found that Nm23-H1 increases the protein stability of hnRNPA2/B1and is thereby co-recruited to the 5'UTR of Sp1 mRNA to regulate cap-independent translational activity. Since the Sp1 level is tightly regulated during lung cancer progression, understanding the molecular mechanisms underlying the regulation by Nm23-H1/hnRNPA2B1 of Sp1 expression in the various stages of lung cancer will be beneficial for lung cancer therapy in the future.

Indexed as

Internal Ribosome Entry Sites5' Untranslated RegionsAgedAnimalsCell Line, TumorCell ProliferationDisease ProgressionDown-RegulationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterogeneous-Nuclear Ribonucleoprotein Group A-BHumansLung NeoplasmsMaleMice5' Untranslated RegionsHeterogeneous-Nuclear Ribonucleoprotein Group A-BhnRNP A2Internal Ribosome Entry SitesNM23 Nucleoside Diphosphate KinasesNME1 protein, humanSP1 protein, humanSp1 Transcription Factor

Identifiers

PMID28831131
PMCPMC5567229
OpenAlexW2749626257

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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.