ArticleHeliyon2023
FLOT1, stabilized by WTAP/IGF2BP2 mediated N6-methyladenosine modification, predicts poor prognosis and promotes growth and invasion in gliomas.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).Molecular medicine reports · 2025Review
- Relationship between CTF1 gene expression and prognosis and tumor immune microenvironment in glioma.European journal of medical research · 2025Article
- The Deep Proteomics Approach Identified Extracellular Vesicular Proteins Correlated to Extracellular Matrix in Type One and Two Endometrial Cancer.International journal of molecular sciences · 2024Article
- Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma.Cells · 2024Review
- Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
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Abstract
The expression, function, and mechanism of FLOT1 (flotillin-1) remains unknown in gliomas. Here, the expression and clinical value of FLOT1 in gliomas was bioinformatically and experimentally analyzed via online omics data and local tissues. Moreover, the effects of FLOT1 depletion on cell proliferation and invasion were also detected. Besides, the underlying roles of N6-methyladenosine modification (m6A) in FLOT1 upregulation was further explored. The results demonstrated that FLOT1 was significantly upregulated in gliomas and positively correlated with advanced progression and poor prognosis of patients. FLOT1 silencing notably suppressed the cell proliferation and invasion in gliomas. The expression of WTAP and IGF2BP2was positively correlated with FLOT1 expression and served as the writer and reader of FLOT1 m6A, respectively, which stabilized FLOT1 mRNA and maintained its upregulation in gliomas. Lastly, ectopic expression of FLOT1 could notably restore the inhibitory effects caused by WTAP and IGF2BP2 depletion in glioma cells. Collectively, our results originally confirmed the upregulation and oncogenic roles of FLOT1, and revealed that WTAP/IGF2BP2 mediated m6A contributed to the upregulation of FLOT1 in gliomas, highlighting the promising application of WTAP/IGF2BP2/FLOT1 axis in target treatment of gliomas.
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