Evidence map›Paper›PMID 40938994›Full record

ArticleScience advances2025

RNA binding protein DDX3X drives pancreatic cancer progression via the TLE2-MYL9 axis.

Yuanyang Wang, Qianyi Yang, Feng Lin, Xiaowei Song, Gang Yang, Dahan Wen, Yingyun Yang, Bicheng Wu, Yunmeng Meng, Ning Zhang and 6 more

Abstract read
In one paragraph

Article in Science advances, 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

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

4 citing papers in PubMed.

  1. Tumor-Derived LAMB3 Drives Immunosuppressive LRRC15Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Article
  4. 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

16 authors.

Yuanyang WangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.ORCID 0000-0003-1898-7897
Qianyi YangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Pharmacology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.ORCID 0000-0002-7767-2767
Feng LinWenzhou Institute, University of Chinese Academy of Sciences, Wenzhou 325001, Zhejiang, China.
Xiaowei SongState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Pharmacology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.ORCID 0009-0007-9060-6469
Gang YangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.ORCID 0000-0001-8641-5925
Dahan WenState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Pharmacology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.
Yingyun YangDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.ORCID 0000-0001-8552-496X
Bicheng WuState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Pharmacology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.
Yunmeng MengState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Pharmacology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.
Ning ZhangInstitute of Blood Transfusion, Peking Union Medical College, Chinese Academy of Medical Sciences, Chengdu 610052, China.ORCID 0000-0003-3934-417X
Xiaomei LuClinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region, PR China.
Chunyang XiongWenzhou Institute, University of Chinese Academy of Sciences, Wenzhou 325001, Zhejiang, China.ORCID 0000-0002-8821-2643
Wen ZhaoDepartment of General Surgery, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Junbo LiangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.ORCID 0000-0001-6230-1421
Taiping ZhangDepartment of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.ORCID 0000-0003-1689-6908
Yuying LiuState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Pharmacology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.ORCID 0000-0003-2182-7210

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current treatments for pancreatic ductal adenocarcinoma (PDAC) fall short of meeting clinical needs, highlighting the urgent need for a comprehensive understanding of PDAC progression, which involves not only biochemical signals but also essential biomechanical cues. Here, we used a CRISPR-Cas9 screen in an orthotopic xenograft model to explore PDAC dynamics. The RNA binding protein DEAD-box helicase 3X-linked (DDX3X) was identified as a pivotal oncogene and biomechanical checkpoint. Specifically, DDX3X up-regulation in PDAC promoted tumorigenesis and metastasis, primarily through the transcriptional repressor TLE family member 2 (TLE2). Dysregulation of DDX3X in the tumor destabilized TLE2 messenger RNA and therefore disrupted the interaction with KLF4 (KLF transcription factor 4), leading to increased expression of myosin light chain 9 (MYL9). This change remodeled F-actin, enhancing tumor cell traction forces and consequently facilitating tumor metastasis. Targeting the DDX3X-TLE2-MYL9 pathway considerably reduces PDAC progression. This research reveals a promising approach for treating PDAC by focusing on biomechanical cues.

Indexed as

Carcinoma, Pancreatic DuctalDEAD-box RNA HelicasesPancreatic NeoplasmsRepressor ProteinsAnimalsCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceSignal TransductionDDX3X protein, humanDEAD-box RNA HelicasesKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsRepressor Proteins

Identifiers

PMID40938994
PMCPMC12429019

What OpenQuestion holds

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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.