Evidence map›Paper›PMID 41926654›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Tetrastigma Hemsleyanum Polysaccharide Suppresses Triple-Negative Breast Cancer by Disrupting the Hippo-YAP/TEAD4-PDIA4 Axis and Endoplasmic Reticulum Stress Adaptation.

Yini Shang, Wentao Si, Youxue Zhang, Jialin Liu, Huaixi Zhang, Yafei Li, Hongmeng Su, Wei Jiang, Zhishan Ding, Lihong Wang

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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

0 citing papers in PubMed.

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

10 authors.

Yini ShangFujian Key Laboratory of Tumor Immunotherapy, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Wentao SiFujian Key Laboratory of Tumor Immunotherapy, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Youxue ZhangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Jialin LiuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Huaixi ZhangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yafei LiSchool of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, China.
Hongmeng SuFujian Key Laboratory of Tumor Immunotherapy, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Wei JiangFujian Key Laboratory of Tumor Immunotherapy, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Zhishan DingSchool of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, China.
Lihong WangFujian Key Laboratory of Tumor Immunotherapy, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID https://orcid.org/0000-0002-6715-2944

Funding

Fujian Provincial Health and Wellness Science and Technology Plan Project 2024GGA037Fujian Provincial Natural Science Foundation 2025J01088Natural Science Foundation of China 62172213Natural Science Foundation of China 62472095
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) exhibits addiction to chronic endoplasmic reticulum (ER) stress, which sustains an aggressive metastatic phenotype through activation of the unfolded protein response (UPR). Here, we identify a previously unrecognized "ER-stress addiction" axis in which the Hippo pathway effector TEAD4 directly transcriptionally upregulates the ER chaperone PDIA4. We further demonstrate that this axis can be pharmacologically targeted by a natural polysaccharide. Tetrastigma hemsleyanum polysaccharide (THP) selectively activates the Hippo kinase cascade, leading to YAP phosphorylation, cytoplasmic sequestration, and subsequent degradation. This cascade attenuates YAP/TEAD4 interaction and abolishes TEAD4 DNA-binding activity. Moreover, THP downregulates TEAD4 expression. These combined effects drive transcriptional suppression of PDIA4, catastrophic disruption of ER proteostasis, and ultimately lethal ER stress in TNBC cells. Functionally, THP inhibits migration, invasion, angiogenesis, and intracellular Ca

Indexed as

Endoplasmic Reticulum StressPolysaccharidesTEA Domain Transcription FactorsTriple Negative Breast NeoplasmsAnimalsCell Line, TumorDNA-Binding ProteinsFemaleHippo Signaling PathwayHumansMiceProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsYAP-Signaling ProteinsZebrafishDNA-Binding ProteinsPolysaccharidesProtein Serine-Threonine KinasesTEAD4 protein, humanTEA Domain Transcription FactorsTranscription FactorsYAP-Signaling Proteinsendoplasmic reticulum stresshippo‐YAP pathwaymetastasistetrastigma hemsleyanum polysaccharidetriple negative breast cancer

Identifiers

PMID41926654
PMCPMC13285156

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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.