Evidence map›Paper›PMID 42286608›Full record

ArticleCell communication and signaling : CCS2026

Liver cancer derived high core fucosylation sEV elict malignancy by activating PI3K/AKT signaling pathway.

Zhuo Li, Na Zhang, Wei Zhang, Jian Zhou, Juan Gao, Xin Wang, Yingjie Ren, Yunjie Wang, Ruiman Geng, Chunyan Yang and 3 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Zhuo Li *Department of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Na Zhang *Department of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Wei Zhang *Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest University, Xi'an, 710069, P.R. China.
Jian ZhouDepartment of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Juan GaoDepartment of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Xin WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Yingjie RenDepartment of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Yunjie WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Ruiman GengDepartment of Laboratory Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, P.R. China.
Chunyan YangInstitute of Hematology, Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, 710021, P.R. China.
Feng GuanKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest University, Xi'an, 710069, P.R. China.
Zhen ZhaiComprehensive Breast Care Center, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, P.R. China.
Lin CaoProvincial Key Laboratory of Biotechnology, School of Medicine, Institute of Hematology, Northwest University, Xi'an, 710069, P.R. China. lincao@nwu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small extracellular vesicles (sEV) play a key role in liver cancer (LC) by supporting cancer cell survival, local invasion, and distant metastasis. Although sEV surfaces are known to be richly glycosylated, how these glycans influence sEV function remains poorly understood. In this study, we observed elevated levels of core fucosylation in LC tissues, serum, and cells, as well as in serum-derived sEV. sEV isolated from highly metastatic MHCC97H cells or from LC patient serum enhanced the proliferation and migration of recipient cells. Conversely, inhibiting core fucosylation on sEV suppressed these malignant phenotypes. Mechanistically, integrated proteomic and glycoproteomic profiling identified lectin galactoside-binding soluble 3-binding protein (LGALS3BP) as significantly enriched in LC serum-derived sEV and modified by core fucosylation. Knockdown of LGALS3BP in donor cells attenuated the malignant behavior of recipient cells by inhibiting PI3K-AKT signaling. Our findings reveal a crucial role for core fucosylation in mediating the pro-tumor functions of LC-derived sEV and suggest that targeting sEV glycosylation may offer a novel therapeutic strategy for LC.

Indexed as

Extracellular VesiclesFucoseLiver NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsAntigens, NeoplasmCarrier ProteinsCell Line, TumorCell MovementCell ProliferationExtracellular Matrix ProteinsGlycoproteinsGlycosylationHumansAntigens, NeoplasmCarrier ProteinsExtracellular Matrix ProteinsFucoseGlycoproteinsLGALS3BP protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCore fucosylationLGALS3BPLiver cancerSmall extracellular vesicle

Identifiers

PMID42286608
PMCPMC13483717

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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.