Evidence map›Paper›PMID 34131109›Full record

ArticleCell death & disease2021

Prrx1 promotes stemness and angiogenesis via activating TGF-β/smad pathway and upregulating proangiogenic factors in glioma.

Zetao Chen, Yihong Chen, Yan Li, Weidong Lian, Kehong Zheng, Yuxuan Zhang, Yujie Zhang, Chuang Lin, Chaoqun Liu, Fei Sun and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  7. Targeting Lipid Metabolism in Cancer Stem Cells for Anticancer Treatment.International journal of molecular sciences · 2024
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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

14 authors at 2 institutions in 1 country.

Zetao Chen *The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.ORCID 0000-0002-9802-8065
Yihong Chen *The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.ORCID 0000-0001-5176-4551
Yan LiThe National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.
Weidong LianThe National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.
Kehong ZhengDivision of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0002-6773-8275
Yuxuan ZhangThe National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.
Yujie ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Chuang LinDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Chaoqun LiuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Fei SunDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xinlin SunThe National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China.
Jihui WangThe National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. 346wangjihui@163.com.ORCID 0000-0001-7586-8873
Liang ZhaoDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. liangsmu@foxmail.com.ORCID 0000-0002-1429-0884
Yiquan KeThe National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. kyquan@smu.edu.cn.ORCID 0000-0002-7356-8559
Zhujiang Hospital · CNNanfang Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81772651National Natural Science Foundation of China (National Science Foundation of China) 81772652National Natural Science Foundation of China (National Science Foundation of China) 81802481National Natural Science Foundation of China (National Science Foundation of China) 82072762
6 · The paper itself

Abstract

Glioma is one of the most lethal cancers with highly vascularized networks and growing evidences have identified glioma stem cells (GSCs) to account for excessive angiogenesis in glioma. Aberrant expression of paired-related homeobox1 (Prrx1) has been functionally associated with cancer stem cells including GSCs. In this study, Prrx1 was found to be markedly upregulated in glioma specimens and elevated Prrx1 expression was inversely correlated with prognosis of glioma patients. Prrx1 potentiated stemness acquisition in non-stem tumor cells (NSTCs) and stemness maintenance in GSCs, accompanied with increased expression of stemness markers such as SOX2. Prrx1 also promoted glioma angiogenesis by upregulating proangiogenic factors such as VEGF. Consistently, silencing Prrx1 markedly inhibited glioma proliferation, stemness, and angiogenesis in vivo. Using a combination of subcellular proteomics and in vitro analyses, we revealed that Prrx1 directly bound to the promoter regions of TGF-β1 gene, upregulated TGF-β1 expression, and ultimately activated the TGF-β/smad pathway. Silencing TGF-β1 mitigated the malignant behaviors induced by Prrx1. Activation of this pathway cooperates with Prrx1 to upregulate the expression of stemness-related genes and proangiogenic factors. In summary, our findings revealed that Prrx1/TGF-β/smad signal axis exerted a critical role in glioma stemness and angiogeneis. Disrupting the function of this signal axis might represent a new therapeutic strategy in glioma patients.

Indexed as

Brain NeoplasmsGliomaAnimalsCells, CulturedChick EmbryoGene Expression Regulation, NeoplasticHEK293 CellsHomeodomain ProteinsHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred BALB CMice, NudeNeoplastic Stem CellsNeovascularization, PathologicHomeodomain ProteinsPRRX1 protein, humanSmad ProteinsTransforming Growth Factor beta1

Identifiers

PMID34131109
PMCPMC8206106
OpenAlexW3171032854

What OpenQuestion holds

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LicenceCC BY
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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.