Evidence map›Paper›PMID 37850692›Full record

ArticleCNS neuroscience & therapeutics2024

A TGF-β signaling-related lncRNA signature for prediction of glioma prognosis, immune microenvironment, and immunotherapy response.

Wei-Wei Duan, Li-Ting Yang, Jian Liu, Zi-Yu Dai, Ze-Yu Wang, Hao Zhang, Xun Zhang, Xi-Song Liang, Peng Luo, Jian Zhang and 6 more

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
24.6field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 103 citations in OpenAlex.

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  19. TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026
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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

16 authors at 6 institutions in 2 countries.

Wei-Wei DuanDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0003-3683-6873
Li-Ting YangDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jian LiuExperiment Center of Medical Innovation, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China.
Zi-Yu DaiDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ze-Yu WangDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Hao ZhangDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xun ZhangDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xi-Song LiangDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Peng LuoDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Jian ZhangDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Zao-Qu LiuDepartment of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Nan ZhangOne-third Lab, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Hei Longjiang, China.
Hao-Yang MoDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Chun-Run QuDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhi-Wei XiaDepartment of Neurology, Hunan Aerospace Hospital, Changsha, Hunan, China.
Quan ChengDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0003-2401-5349
Central South University · CNZhujiang Hospital · CNFirst Affiliated Hospital of Hunan University of Traditional Chinese Medicine · CNFirst Affiliated Hospital of Zhengzhou University · CNHarbin Medical University · CNHunan Mawangdui Hospital · CN

Funding

Hunan Provincial Health Committee Foundation of China 202204044869Hunan Provincial Natural Science Foundation of China 2019JJ50780Hunan Provincial Natural Science Foundation of China 2022JJ20095National Natural Science Foundation of China 81903015National Natural Science Foundation of China 82073893Science Foundation of AMHT Group 2022YK04
6 · The paper itself

Abstract

aimsThe dysregulation of TGF-β signaling is a crucial pathophysiological process in tumorigenesis and progression. LncRNAs have diverse biological functions and are significant participants in the regulation of tumor signaling pathways. However, the clinical value of lncRNAs related to TGF-β signaling in glioma is currently unclear.

methodsData on glioma's RNA-seq transcriptome, somatic mutation, DNA methylation data, and clinicopathological information were derived from the CGGA and TCGA databases. A prognostic lncRNA signature was constructed by Cox and LASSO regression analyses. TIMER2.0 database was utilized to deduce immune infiltration characteristics. "ELMER v.2" was used to reconstruct TF-methylation-gene regulatory network. Immunotherapy and chemotherapy response predictions were implemented by the TIDE algorithm and GDSC database, respectively. In vitro and in vivo experiments were conducted to verify the results and clarify the regulatory mechanism of lncRNA.

resultsIn glioma, a TGF-β signaling-related 15-lncRNA signature was constructed, including AC010173.1, HOXA-AS2, AC074286.1, AL592424.1, DRAIC, HOXC13-AS, AC007938.1, AC010729.1, AC013472.3, AC093895.1, AC131097.4, AL606970.4, HOXC-AS1, AGAP2-AS1, and AC002456.1. This signature proved to be a reliable prognostic tool, with high risk indicating an unfavorable prognosis and being linked to malignant clinicopathological and genomic mutation traits. Risk levels were associated with different immune infiltration landscapes, where high risk was indicative of high levels of macrophage infiltration. In addition, high risk also suggested better immunotherapy and chemotherapy response. cg05987823 was an important methylation site in glioma progression, and AP-1 transcription factor family participated in the regulation of signature lncRNA expression. AGAP2-AS1 knockdown in in vitro and in vivo experiments inhibited the proliferation, migration, and invasion of glioma cells, as well as the growth of glioma, by downregulating the expression levels of NF-κB and ERK 1/2 in the TGF-β signaling pathway.

conclusionsA prognostic lncRNA signature of TGF-β signaling was established in glioma, which can be used for prognostic judgment, immune infiltration status inference, and immunotherapy response prediction. AGAP2-AS1 plays an important role in glioma progression.

Indexed as

GliomaRNA, Long NoncodingTransforming Growth Factor betaHumansImmunotherapyNF-kappa BPrognosisTumor MicroenvironmentNF-kappa BRNA, Long NoncodingTransforming Growth Factor betagliomaimmune infiltrationimmunotherapylncRNAprognosisTGF‐β

Identifiers

PMID37850692
PMCPMC11017415
OpenAlexW4387729011

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.