Evidence map›Paper›PMID 28216662›Full record

ArticleScientific reports2017

DDX5 promotes gastric cancer cell proliferation in vitro and in vivo through mTOR signaling pathway.

Cheng Du, Dan-Qi Li, Na Li, Li Chen, Shi-Sen Li, Yang Yang, Ming-Xiao Hou, Man-Jiang Xie, Zhen-Dong Zheng

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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. DEAD/H-box RNA helicase 10 promotes pancreatic cancer cell proliferationWorld journal of gastrointestinal oncology · 2025
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  13. NAR cancer · 2022
    Article
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  17. Article
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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

9 authors at 4 institutions in 1 country.

Cheng DuDepartment of Oncology, General Hospital of Shenyang Military Area Command, Shenyang 110840, P. R. China.
Dan-Qi LiInstitute of Functional Molecules, Shenyang University of Chemical Technology, Shenyang 110142, P. R. China.
Na LiDepartment of Gynaecology and Obstetrics, First Affiliated Hospital, Jilin University, Jilin 130021, P. R. China.
Li ChenDepartment of Aerospace Medicine, The Fourth Military Medical University, Xi'an 710032, P. R. China.
Shi-Sen LiDepartment of Digestive Surgery, Xijing Hospital of Digestive Diseases, The Fourth Military Medical University, Xi'an 710032, China.
Yang YangDepartment of Oncology, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, P. R. China.
Ming-Xiao HouRescue Center of Severe Wound and Trauma of PLA, General Hospital of Shenyang Military Area Command, Shenyang 110840, P. R. China.
Man-Jiang XieDepartment of Aerospace Medicine, The Fourth Military Medical University, Xi'an 710032, P. R. China.
Zhen-Dong ZhengDepartment of Oncology, General Hospital of Shenyang Military Area Command, Shenyang 110840, P. R. China.
Air Force Medical University · CNGeneral Hospital of Shenyang Military Region · CNJilin University · CNShenyang University of Chemical Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DEAD (Asp-Glu-Ala-Asp) box helicase 5 (DDX5) is an ATP-dependent RNA helicase that is overexpressed in various malignancies. Increasing evidence suggests that DDX5 participates in carcinogenesis and cancer progression via promoting cell proliferation and metastasis. However, the functional role of DDX5 in gastric cancer is largely unknown. In this study, we observed that DDX5 was significantly up-regulated in gastric cancer tissues compared with the paired adjacent normal tissues. The expression of DDX5 correlated strongly with Ki67 index and pathological stage of gastric cancer. In vitro and in vivo studies suggested that knockdown of DDX5 inhibited gastric cancer cell proliferation, colony formation and xenografts growth, whereas ectopic expression of DDX5 promoted these cellular functions. Mechanically, DDX5 induced gastric cancer cell growth by activating mTOR/S6K1. Treatment of everolimus, the specific mTOR inhibitor, significantly attenuated DDX5-mediated cell proliferation. Interestingly, the expression of DDX5 and p-mTOR in gastric cancer tissues demonstrated a positive correlation. Taken together, these results revealed a novel role of DDX5 in gastric cancer cell proliferation via the mTOR pathway. Therefore, DDX5 may serve as a therapeutic target in gastric cancer.

Indexed as

Signal TransductionUp-RegulationAnimalsCell Line, TumorCell ProliferationDEAD-box RNA HelicasesEverolimusGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceNeoplasm StagingNeoplasm TransplantationRibosomal Protein S6 Kinases, 70-kDaStomach NeoplasmsTOR Serine-Threonine KinasesDdx5 protein, humanDEAD-box RNA HelicasesEverolimusMTOR protein, humanribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine Kinases

Identifiers

PMID28216662
PMCPMC5316961
OpenAlexW2591378684

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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.