Evidence map›Paper›PMID 39289531›Full record

ArticleOncogene2024

DDX5 promotes esophageal squamous cell carcinoma growth through sustaining VAV3 mRNA stability.

Yunshu Shi, Junyong Wang, Qiang Yuan, Yingying Chen, Miao Zhao, Xiaoyu Li, Zitong Wang, Hao Zhou, Fangli Zhu, Bing Wei and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. [Performance of Plasma Multigene Methylation Testing in Early Diagnosis of Colorectal Cancer].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    Article
  5. Article
  6. Article
  7. Review
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

15 authors.

Yunshu ShiThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Junyong WangAcademy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Qiang YuanThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Yingying ChenThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Miao ZhaoThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Xiaoyu LiThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Zitong WangThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Hao ZhouThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Fangli ZhuThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Bing WeiDepartment of Molecule and Pathology, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan, China.
Yanan JiangThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.ORCID 0000-0001-6129-643X
Jimin ZhaoThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.ORCID 0000-0002-3338-9994
Yan QiaoThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China. yanqiao@zzu.edu.cn.ORCID 0000-0001-6357-8203
Zigang DongThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China. zgdong@hci-cn.org.ORCID 0000-0002-4174-4028
Kangdong LiuThe Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China. kdliu@zzu.edu.cn.ORCID 0000-0002-4425-5625

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81872335National Natural Science Foundation of China (National Science Foundation of China) 82472998
6 · The paper itself

Abstract

Novel therapeutic targets and their inhibitors for esophageal squamous cell carcinoma (ESCC) prevention and therapy are urgently needed. This study aimed to investigate the function of DEAD-box helicase 5 (DDX5) in ESCC progression and to identify a promising inhibitor of DDX5. We verified that DDX5 was highly expressed in ESCC and played an oncogenic role, binding with vav guanine nucleotide exchange factor 3 (VAV3) mRNA and facilitating VAV3 mRNA N6-methyladenosine (m6A) modification by interacting with the m6A methyltransferase 3 (METTL3). M6A-modified VAV3 mRNA was identified by insulin-like growth factor 1 (IGF2BP1), increasing mRNA stability. Methylnissolin-3-β-D-O-glucoside (MD) inhibited ESCC progression through the DDX5-VAV3 axis. Our findings suggest that DDX5 promotes ESCC progression. MD inhibits ESCC progression by targeting DDX5.

Indexed as

DEAD-box RNA HelicasesEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaProto-Oncogene Proteins c-vavRNA StabilityAdenosineAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMethyltransferasesMiceAdenosineDdx5 protein, humanDEAD-box RNA HelicasesMethyltransferasesMETTL3 protein, humanProto-Oncogene Proteins c-vavRNA, MessengerVAV3 protein, human

Identifiers

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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.