Evidence map›Paper›PMID 40394670›Full record

ArticleJournal of translational medicine2025

YY1-induced DDX18 modulates EMT via the AKT/mTOR pathway in esophageal cancer: a novel therapeutic target.

Xiaochao Ma, Yulu He, Yue Yang, Tianyu Lu, Ze Tang, Youbin Cui, Rui Wang

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xiaochao MaDepartment of Thoracic Surgery, Organ Transplantation Center, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, Jilin, 130021, China.
Yulu HeGenetic Diagnosis Center, The First Hospital of Jilin University, Changchun, Jilin, 130021, China.
Yue YangDepartment of Thoracic Surgery, Organ Transplantation Center, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, Jilin, 130021, China.
Tianyu LuDepartment of Thoracic Surgery, Organ Transplantation Center, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, Jilin, 130021, China.
Ze TangDepartment of Thoracic Surgery, Organ Transplantation Center, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, Jilin, 130021, China.
Youbin CuiDepartment of Thoracic Surgery, Organ Transplantation Center, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, Jilin, 130021, China. cuiyb@jlu.edu.cn.
Rui WangDepartment of Thoracic Surgery, Organ Transplantation Center, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, Jilin, 130021, China. ruiwang14@mails.jlu.edu.cn.

Funding

Jilin Provincial Scientific and Technological Development Program 20130604050TC
6 · The paper itself

Abstract

backgroundEsophageal cancer is the 11th most common malignancy and the 7th leading cause of cancer-related death globally. Identifying key molecules and underlying mechanisms in the progression of esophageal cancer represents an effective strategy for developing novel therapeutic approaches.

methodsDDX18 expression in clinical specimens was evaluated by immunohistochemistry and western blot analysis. Functional assays were performed in cells with either DDX18 knockdown or overexpression. Dual luciferase reporter assays and chromatin immunoprecipitation (ChIP) were conducted to validate the interaction between YY1 and the DDX18 promoter. A xenograft tumor model was utilized to investigate the role of DDX18 in vivo in esophageal cancer.

resultsDDX18 was found to be markedly overexpressed in esophageal cancer, with its levels significantly higher in patients with pathological grade III compared to those with grades I-II. In vitro, DDX18 enhanced cell proliferation, migration, and invasion, while concurrently suppressing apoptosis. Furthermore, DDX18 promoted epithelial-mesenchymal transition (EMT) and activated the AKT/mTOR signaling pathway. The use of AKT inhibitors effectively abrogated the oncogenic effects of DDX18. Dual luciferase and ChIP assays confirmed that YY1 binds to and stimulates DDX18 transcription. In rescue experiments, YY1 countered the inhibitory effects of DDX18 knockdown on cell proliferation, EMT, and AKT/mTOR activation. In vivo, DDX18 knockdown resulted in reduced tumor growth.

conclusionsThe transcription of DDX18 was activated by YY1, and DDX18 promoted tumor cell growth and EMT through the AKT/mTOR signaling pathway in esophageal cancer cells.

Indexed as

DEAD-box RNA HelicasesEpithelial-Mesenchymal TransitionEsophageal NeoplasmsMolecular Targeted TherapyProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesYY1 Transcription FactorAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansDEAD-box RNA HelicasesMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesYY1 protein, humanYY1 Transcription FactorApoptosisDDX18EMTEsophageal cancerTranscription factor

Identifiers

PMID40394670
PMCPMC12090415

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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.