Evidence map›Paper›PMID 42070227›Full record

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

GLS1 Orchestrates Exosome-Mediated Tumor-Endothelial Communication to Facilitate Angiogenesis.

Jianqiang Yang, Zhenzhen Fu, Fanghui Chen, Soumya Vijaya Kumar, Fan Yang, Yaochao Zheng, Yunqi Li, Yao Yao, Nabil F Saba, Yong Teng

Abstract read
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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
–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

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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

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.

Jianqiang YangDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.
Zhenzhen FuDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.
Fanghui ChenDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.
Soumya Vijaya KumarDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.
Fan YangDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.
Yaochao ZhengRegenerative Bioscience Center, Department of Animal and Dairy Science, University of Georgia, Athens, Georgia, USA.ORCID https://orcid.org/0000-0003-1646-5964
Yunqi LiDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.
Yao YaoRegenerative Bioscience Center, Department of Animal and Dairy Science, University of Georgia, Athens, Georgia, USA.
Nabil F SabaDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.ORCID https://orcid.org/0000-0003-4972-1477
Yong TengDepartment of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, Georgia, USA.ORCID https://orcid.org/0000-0002-1856-7289

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Gregory B. Lesinski · 2009 to 2026
$47.5M
Inhibiting mitochondrial complex I to improve cetuximab efficacy in oral cancerR01DE033691 · NIDCR · EMORY UNIVERSITY · PI Yong Teng · 2024 to 2026
$1.2M
Targeted Arf1 inhibition to enhance immune response in oral cancerR01DE033433 · NIDCR · EMORY UNIVERSITY · PI Yong Teng · 2024 to 2026
$1.1M
CMB Pilot Award P30CA138292NCI NIH HHS P30 CA138292NIDCR NIH HHS R01 DE033433NIDCR NIH HHS R01 DE033691NIH/NIDCR R01DE033433NIH/NIDCR R01DE033691Winship Invest$ Pilot Award P30CA138292Winship Invest$ Team Science Award P30CA138292
6 · The paper itself

Abstract

Glutaminase 1 (GLS1) drives glutaminolysis to support tumor growth and survival, yet its role in the tumor microenvironment remains poorly understood. Here, we demonstrate that GLS1 promotes angiogenesis in head and neck squamous cell carcinoma (HNSCC) via an exosome-dependent mechanism. In HNSCC xenograft models, genetic silencing of GLS1 or treatment with CB-839 markedly reduces intratumoral angiogenesis. Exosomes from GLS1-deficient cells impair endothelial cell migration and tube formation compared with control exosomes. Proteomic analysis reveals a loss of the pro-angiogenic protein Tenascin C (TNC) in GLS1-deficient exosomes. Mechanistically, loss of GLS1 interferes with USP1-mediated deubiquitination of Caveolin-1 (CAV1), resulting in CAV1 degradation and impaired recruitment of TNC into exosomes. Exosomes deficient in CAV1-TNC complexes subsequently disrupt integrin-dependent FAK-SRC signaling in endothelial cells, inhibiting their angiogenic activity. Collectively, these findings uncover a non-metabolic role of GLS1 in promoting tumor angiogenesis through exosome-mediated CAV1-TNC signaling, suggesting that targeting GLS1 may simultaneously inhibit tumor metabolism and angiogenesis in HNSCC.

Indexed as

ExosomesGlutaminaseHead and Neck NeoplasmsNeovascularization, PathologicSquamous Cell Carcinoma of Head and NeckAnimalsCaveolin 1Cell CommunicationCell Line, TumorCell MovementEndothelial CellsHumansMiceSignal TransductionTumor MicroenvironmentCaveolin 1GLS protein, humanGlutaminaseangiogenesisCAV1‐TNC signalingexosomesGLS1HNSC

Identifiers

PMID42070227
PMCPMC13335626

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.