Evidence map›Paper›PMID 36045101›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

Bladder Cancer-Derived Small Extracellular Vesicles Promote Tumor Angiogenesis by Inducing HBP-Related Metabolic Reprogramming and SerRS O-GlcNAcylation in Endothelial Cells.

Xinyuan Li, Xiang Peng, Chunlin Zhang, Xuesong Bai, Yang Li, Guo Chen, Huixia Guo, Weiyang He, Xiang Zhou, Xin Gou

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
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

35 citing papers in PubMed, 45 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Xinyuan LiDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.ORCID 0000-0001-8385-8691
Xiang PengDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Chunlin ZhangDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xuesong BaiDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yang LiDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Guo ChenDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Huixia GuoCentre for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, 200031, China.
Weiyang HeDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiang ZhouDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xin GouDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNChinese Academy of Sciences · CN

Funding

Chongqing Science and Technology Bureau cstc2019jscx-dxwtBX0018National Natural Science Foundation of China 81874092
6 · The paper itself

Abstract

A malformed tumour vascular network provokes the nutrient-deprived tumour microenvironment (TME), which conversely activates endothelial cell (EC) functions and stimulates neovascularization. Emerging evidence suggests that the flexible metabolic adaptability of tumour cells helps to establish a metabolic symbiosis among various cell subpopulations in the fluctuating TME. In this study, the authors propose a novel metabolic link between bladder cancer (BCa) cells and ECs in the nutrient-scarce TME, in which BCa-secreted glutamine-fructose-6-phosphate aminotransferase 1 (GFAT1) via small extracellular vesicles (sEVs) reprograms glucose metabolism by increasing hexosamine biosynthesis pathway flux in ECs and thus enhances O-GlcNAcylation. Moreover, seryl-tRNA synthetase (SerRS) O-GlcNAcylation at serine 101 in ECs promotes its degradation by ubiquitination and impeded importin α5-mediated nuclear translocation. Intranuclear SerRS attenuates vascular endothelial growth factor transcription by competitively binding to the GC-rich region of the proximal promotor. Additionally, GFAT1 knockout in tumour cells blocks SerRS O-GlcNAcylation in ECs and attenuates angiogenesis both in vitro and in vivo. However, administration of GFAT1-overexpressing BCa cells-derived sEVs increase the angiogenetic activity in the ECs of GFAT1-knockout mice. In summary, this study suggests that inhibiting sEV-mediated GFAT1 secretion from BCa cells and targeting SerRS O-GlcNAcylation in ECs may serve as novel strategies for BCa antiangiogenetic therapy.

Indexed as

Extracellular VesiclesSerine-tRNA LigaseUrinary Bladder NeoplasmsAnimalsEndothelial CellsGlucoseGlutamine-Fructose-6-Phosphate Transaminase (Isomerizing)HexosaminesKaryopherinsMiceSerineTumor MicroenvironmentVascular Endothelial Growth Factor AGlucoseGlutamine-Fructose-6-Phosphate Transaminase (Isomerizing)HexosaminesKaryopherinsSerineSerine-tRNA LigaseVascular Endothelial Growth Factor Aangiogenesisglutamine-fructose-6-phosphate aminotransferase 1metabolic reprogrammingO-GlcNAcylationsmall extracellular vesicles

Identifiers

PMID36045101
PMCPMC9596856
OpenAlexW4294128602

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.