Evidence map›Paper›PMID 29535419›Full record

ArticleOncogene2018

DEAD-box helicase 27 promotes colorectal cancer growth and metastasis and predicts poor survival in CRC patients.

Jieting Tang, Huarong Chen, Chi-Chun Wong, Dabin Liu, Tong Li, Xiaohong Wang, Jiafu Ji, Joseph Jy Sung, Jing-Yuan Fang, Jun Yu

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. METTL3 loss exacerbates colitis via mActa pharmacologica Sinica · 2026
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  4. RNA mCancer communications (London, England) · 2025
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  9. Review
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  11. miR-617 interacts with the promoter ofFrontiers in oncology · 2024
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  12. Review
  13. Article
  14. METTL3-ModulatedCancers · 2023
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  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

10 authors at 5 institutions in 1 country.

Jieting TangInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Huarong ChenInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Chi-Chun WongInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Dabin LiuInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Tong LiInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Xiaohong WangDepartment of Surgery, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Jiafu JiDepartment of Surgery, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Joseph Jy SungInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Jing-Yuan FangState Key Laboratory for Oncogenes and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Cancer Institute,Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, 200001, China. jingyuanfang@sjtu.edu.cn.
Jun YuInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China. junyu@cuhk.edu.hk.
Chinese University of Hong Kong · CNPeking University · CNPrince of Wales Hospital · CNShanghai Jiao Tong University · CNChinese University of Hong Kong, Shenzhen · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copy number alterations (CNAs) are crucial for colorectal cancer (CRC) development. In this study, DEAD box polypeptide 27 (DDX27) was identified to be highly amplified in both TCGA CRC (474/615) and primary CRC (47/103), which was positively correlated with its mRNA overexpression. High DDX27 mRNA (N = 199) and protein expression (N = 260) predicted poor survival in CRC patients. Ectopic expression of DDX27 increased CRC cells proliferation, migration and invasion, but suppressed apoptosis. Conversely, silencing of DDX27 exerted opposite effects in vitro and significantly inhibited murine xenograft tumor growth and lung metastasis in vivo. Up-regulation of DDX27 enhanced and prolonged TNF-α-mediated NF-κB signaling. Nucleophosmin (NPM1) was identified as a binding partner of DDX27. DDX27 increased nuclear NPM1 and NF-κB-p65 interaction to enhance DNA binding activity of NF-κB. Silencing NPM1 abrogated DDX27-activating NF-κB signaling and its tumor-promoting function. Together, DDX27 is overexpressed and plays a pivotal oncogenic role in CRC.

Indexed as

AnimalsCell Line, TumorCell MovementCell NucleusCell ProliferationColorectal NeoplasmsDEAD-box RNA HelicasesGene DosageGene Expression Regulation, NeoplasticHCT116 CellsHumansLung NeoplasmsMiceNeoplasm TransplantationNF-kappa BNuclear ProteinsDDX27 protein, humanDEAD-box RNA HelicasesNF-kappa BNPM1 protein, humanNpm1 protein, mouseNuclear ProteinsNucleophosminTumor Necrosis Factor-alpha

Identifiers

PMID29535419
PMCPMC5978808
OpenAlexW2789724703

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.