Evidence map›Paper›PMID 42694796›Full record

ArticleInternational journal of biological sciences2026

The Acidic Exosomal miR-1246/WASF3 Axis Regulates Hepatic Stellate Cell Activation and Stiff ECM Remodeling to Promote Pancreatic Ductal Adenocarcinoma Liver Metastasis.

Dongqi Li, Xiangyu Chu, Fusheng Zhang, Yongsu Ma, Weikang Liu, Ping Li, Xiaocui Fang, Chen Wang, Xiaodong Tian, Yanlian Yang and 1 more

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Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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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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

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No citing paper in PubMed yet.

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

11 authors.

Dongqi LiDepartment of Hepatobiliary ad Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China.
Xiangyu ChuDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, State Key Lab of Digestive Health, National Clinical Research Center for Digestive Diseases, Beijing, 100050, China.
Fusheng ZhangDepartment of Hepatobiliary ad Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China.
Yongsu MaDepartment of Hepatobiliary ad Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China.
Weikang LiuDepartment of Hepatobiliary ad Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China.
Ping LiCAS Key Laboratory of Standardization and Measurement for Nanotechnology, CAS Key Laboratory of Biological Effects of Nanomaterials and Nanosafety, National Center for Nanoscience and Technology, Beijing, China.
Xiaocui FangCAS Key Laboratory of Standardization and Measurement for Nanotechnology, CAS Key Laboratory of Biological Effects of Nanomaterials and Nanosafety, National Center for Nanoscience and Technology, Beijing, China.
Chen WangCAS Key Laboratory of Standardization and Measurement for Nanotechnology, CAS Key Laboratory of Biological Effects of Nanomaterials and Nanosafety, National Center for Nanoscience and Technology, Beijing, China.
Xiaodong TianDepartment of Hepatobiliary ad Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China.
Yanlian YangCAS Key Laboratory of Standardization and Measurement for Nanotechnology, CAS Key Laboratory of Biological Effects of Nanomaterials and Nanosafety, National Center for Nanoscience and Technology, Beijing, China.
Yinmo YangDepartment of Hepatobiliary ad Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver metastasis is a major factor contributing to the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). The formation of pre-metastatic niche (PMN) initiates the process of liver metastasis. Exosomes (Exos) act as key mediators of crosstalk between the tumor microenvironment (TME) and the PMN to activate hepatic stellate cells (HSCs) and remodel the stiff extracellular matrix (ECM). In this study, we isolated Exos derived from PDAC cells cultured under acidic conditions and demonstrated that these Exos significantly activate HSCs and promote the remodeling of the stiff ECM, thereby promoting the stemness, migration, and invasion of PDAC cells. High expression of exosomal miR-1246 was screened by miRNA-sequencing, and Wiskott-Aldrich syndrome protein Family Member 3 (WASF3) was identified as the target of miR-1246. Mechanistically, exosomal miR-1246 activates HSCs to remodel the ECM by targeting WASF3 and stimulating the phosphatidylinositol 3-kinase-serine/threonine protein kinase (PI3K/Akt) pathway. Notably, RNA-binding protein immunoprecipitation (RIP) and miRNA pull-down assays were performed to identify that Human Antigen R (HuR) contributes to the enrichment of miR-1246 into Exos. Collectively, exosomal miR-1246 activates HSCs and remodels the stiff ECM to promote liver metastasis, and it may serve as a potential diagnostic and prognostic marker for PDAC liver metastasis.

Indexed as

Carcinoma, Pancreatic DuctalExosomesExtracellular MatrixHepatic Stellate CellsLiver NeoplasmsMicroRNAsPancreatic NeoplasmsWiskott-Aldrich Syndrome ProteinAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceSignal TransductionTumor MicroenvironmentWiskott-Aldrich Syndrome Protein FamilyMicroRNAsMIRN1246 microRNA, humanWASF3 protein, humanWiskott-Aldrich Syndrome ProteinWiskott-Aldrich Syndrome Protein FamilyExosomal miRNALiver metastasisPancreatic ductal adenocarcinomapre-metastatic nicheStiff extracellular matrix

Identifiers

PMID42694796
PMCPMC13541008

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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.