Evidence map›Paper›PMID 42897630›Full record

ArticleCancer cell international2026

Quantitative proteomic landscape reveals the role of CSPG5 in the recurrence of glioma.

Shijian Wang, Baorui Tian, Huimin Liu, Chen Zhang, Jianan Wang, Xin Song, Ruibing Li, Haoran Guo, Nan Wang, Wanjun Zhang and 3 more

Abstract read
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In one paragraph

Article in Cancer cell international, 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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1 · What the graph read from it

What it found

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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

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4 · The record

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5 · Who and what money

Authors and funding

13 authors.

Shijian Wang *The School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China.
Baorui Tian *Department of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Huimin Liu *The School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China.
Chen ZhangThe School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China.
Jianan WangDepartment of Laboratory Medicine, the First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Xin SongDepartment of Pathology, the First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Ruibing LiDepartment of Laboratory Medicine, the First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Haoran GuoDepartment of Laboratory Medicine, the First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Nan WangThe Second Surgical Department of Breast Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Wanjun ZhangState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Yongjun PiaoThe School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China.
Yi ShiThe School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China. yishi@nankai.edu.cn.
Rong XiangThe School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, China. rxiang@nankai.edu.cn.

Funding

National Key Research and Development Program of China 2021YFC2401105National Natural Science Foundation of China 82373033Natural Science Foundation of Inner Mongolia Autonomous Region 2020MS01819
6 · The paper itself

Abstract

backgroundThe high recurrence rate of glioma accounts for the majority of glioma-related deaths. Although numerous studies have investigated genomic and transcriptomic alterations, high-resolution quantitative proteomic profiling studies remain limited.

methodsA total of 63 pairs of primary and recurrent formalin-fixed paraffin-embedded glioma tissues (WHO grade II-IV) were collected. Proteomic profiles were generated by data-independent acquisition mass spectrometry (DIA-MS). Differentially expressed proteins were validated using publicly available databases, immunohistochemistry, and Western blotting. The effects of CSPG5 on glioma cell proliferation and invasion were assessed in vitro and in an orthotopic mouse model. Protein-protein interactions were examined by co-immunoprecipitation, and the influence of CSPG5 on ErbB2 degradation was evaluated by immunofluorescence and quantitative PCR.

resultsTwo distinct proteomic clusters (Cluster 1 and Cluster 2) associated with glioma recurrence were identified. Chondroitin sulfate proteoglycan 5 (CSPG5) was markedly down-regulated in recurrent tumors. Overexpression of CSPG5 significantly inhibited glioma cell proliferation and invasion in vitro and reduced tumor burden in vivo. Mechanistically, CSPG5 interacted with ErbB2 and promoted its lysosomal degradation, leading to attenuated PI3K-AKT and ERK signaling.

conclusionsCSPG5 acts as a novel suppressor of ErbB2 signaling; its loss facilitates ErbB2 hyperactivation and thereby promotes glioma recurrence.

Indexed as

CSPG5ErbB signaling pathwayGlioma recurrenceLysosomal degradationPrognostic biomarker

Identifiers

PMID42897630
PMCPMC13681961

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