Evidence map›Paper›PMID 27198888›Full record

ArticleScientific reports2016

The DEAD-box RNA helicase 51 controls non-small cell lung cancer proliferation by regulating cell cycle progression via multiple pathways.

Xiaojing Wang, Hongli Liu, Chengling Zhao, Wei Li, Huanbai Xu, Yuqing Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Role of DEAD/DEAH-box helicases in immunity, infection and cancers.Cell communication and signaling : CCS · 2025
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. RNA Helicases as Shadow Modulators of Cell Cycle Progression.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Live kinase B1 maintains CD34Molecular and cellular biochemistry · 2017
    Article
  10. Article
  11. Review
  12. DDX51 gene promotes proliferation by activating Wnt/β-catenin signaling in breast cancer.International journal of clinical and experimental pathology · 2017
    Article
  13. 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

6 authors at 3 institutions in 1 country.

Xiaojing WangDepartment of Respiration; Anhui Clinical and Preclinical Key Laboratory of Respiratory Diseases; First Affiliated Hospital; Bengbu Medical College; Bengbu 233000, Anhui China.
Hongli LiuDepartment of Gynecological Oncology, First Affiliated Hospital; Bengbu Medical College; Bengbu 233000, Anhui China.
Chengling ZhaoDepartment of Respiration; Anhui Clinical and Preclinical Key Laboratory of Respiratory Diseases; First Affiliated Hospital; Bengbu Medical College; Bengbu 233000, Anhui China.
Wei LiDepartment of Respiration; Anhui Clinical and Preclinical Key Laboratory of Respiratory Diseases; First Affiliated Hospital; Bengbu Medical College; Bengbu 233000, Anhui China.
Huanbai XuDepartment of Endocrinology and Metabolism, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, China.
Yuqing ChenDepartment of Respiration; Anhui Clinical and Preclinical Key Laboratory of Respiratory Diseases; First Affiliated Hospital; Bengbu Medical College; Bengbu 233000, Anhui China.
Bengbu Medical College · CNFirst Affiliated Hospital of Chinese PLA General Hospital · CNShanghai First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The genetic regulation of cell cycle progression and cell proliferation plays a role in the growth of non-small cell lung cancer (NSCLC), one of the most common causes of cancer-related mortality. Although DEAD-box RNA helicases are known to play a role in cancer development, including lung cancer, the potential involvement of the novel family member DDX51 has not yet been investigated. In the current study we assessed the role of DDX51 in NSCLC using a siRNA-based approach. DDX51 siRNA-expressing cells exhibited a slower cell proliferation rate and underwent arrest in S-phase of the cell cycle compared with control cells. Microarray analyses revealed that DDX51siRNA expression resulted in the dysregulation of a number of cell signalling pathways. Moreover, injection of DDX51 siRNA into an animal model resulted in the formation of smaller tumours compared with the control group. We also assessed the expression of DDX51 in patients with NSCLC, and the data revealed that the expression was correlated with patient age but no other risk factors. Overall, our data suggest for the first time that DDX51 aids cell cancer proliferation by regulating multiple signalling pathways, and that this protein might be a therapeutic target for NSCLC.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell ProliferationDEAD-box RNA HelicasesFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMiddle AgedRNA, Small InterferingDDX51 protein, humanDEAD-box RNA HelicasesRNA, Small Interfering

Identifiers

PMID27198888
PMCPMC4873746
OpenAlexW2397395972

What OpenQuestion holds

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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.