Evidence map›Paper›PMID 41555358›Full record

ArticleBMC medical genomics2026

TMEM201 regulates tumor malignancy and immune microenvironment in lower-grade glioma.

Fei Shen, Shanshan Guo

Abstract read
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Article in BMC medical genomics, 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

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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

2 authors.

Fei ShenDepartment of Ophthalmology, Kaifeng Key Laboratory of Cataract and Myopia and Kaifeng Eye Hospital, Kaifeng Central Hospital, Kaifeng, Henan, China.
Shanshan GuoDepartment of Ophthalmology, Kaifeng Key Laboratory of Cataract and Myopia and Kaifeng Eye Hospital, Kaifeng Central Hospital, Kaifeng, Henan, China. guoshankaifeng@outlook.com.ORCID http://orcid.org/0009-0005-9737-8302

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTMEM201, a nuclear membrane protein, is thought to play an important role in tumor progression, but its involvement in lower-grade glioma (LGG) remains unclear. This study aims to investigate the impact of TMEM201 expression on the prognosis, clinical characteristics, and biological behaviors of LGG.

methodsRNA expression data from the TCGA, CGGA, and GEO databases were analyzed to explore the correlation between TMEM201 expression and clinical features of LGG. In vitro and in vivo experiments were conducted to assess the effects of TMEM201 knockdown on cell proliferation, migration, and tumorigenic potential. DNA methylation sites associated with TMEM201 were analyzed, and KEGG pathway enrichment was performed to identify the molecular mechanisms underlying TMEM201’s role in LGG.

resultsThe analysis showed that high TMEM201 expression was associated with poor prognosis, higher WHO grade, and tumor recurrence in LGG patients. Survival analysis confirmed that elevated TMEM201 levels correlated with shorter survival. Knockdown of TMEM201 in SHG44 cells led to significant inhibition of cell proliferation, migration, and tumor formation in vivo. DNA methylation analysis identified key sites regulating TMEM201 expression, and KEGG analysis revealed pathways such as HIF-1, VEGF, and Notch that contribute to tumor progression.

conclusionTMEM201 acts as a potential oncogene in LGG by influencing key cellular signaling pathways and tumor behaviors. It is an independent risk factor for poor prognosis and may serve as a promising biomarker for diagnosis and personalized treatment. This study provides valuable insights into the molecular mechanisms of LGG progression and highlights TMEM201 as a therapeutic target.

Indexed as

Brain NeoplasmsGliomaMembrane ProteinsTumor MicroenvironmentAnimalsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDNA MethylationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm GradingBiomarkers, TumorMembrane ProteinsDNA methylationImmune microenvironmentLower-grade glioma(LGG)OncogenePrognosisTMEM201

Identifiers

PMID41555358
PMCPMC12908378

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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.