ArticleJournal of molecular neuroscience : MN2022
CircRFX3 Up-regulates Its Host Gene RFX3 to Facilitate Tumorigenesis and Progression of Glioma.
Article in Journal of molecular neuroscience : MN, 2022. 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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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Single-cell analysis identifies dysregulated cell type-specific gene programs and intercellular crosstalk underlying colorectal cancer.NPJ precision oncology · 2026Article
- Multifaceted functions of transcription regulatory factor X6 (RFX6): from pancreatic development to cancer progression.Cancer cell international · 2025Review
- Cell cycle-related biomarker lineage promotes the malignant progression of recurrent IDH wild-type glioma.Discover oncology · 2025Article
- Pan-cancer investigation of RFX family and associated genes identifies RFX8 as a therapeutic target in leukemia.Heliyon · 2024Article
- Cuproptosis signature and PLCD3 predicts immune infiltration and drug responses in osteosarcoma.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGlioma is classified as one of the most common types of primary brain tumors. The high expression of CircRFX3 has been found in glioma. However, its functional roles in glioma and underlying mechanism remain unknown. PURPOSE: Our study aimed to explore the function and specific mechanism of circRFX3 in glioma.
methodsRT-qPCR or western blot was applied to examine the expression of RNAs or proteins. Functional assays were carried out to evaluate the influence of circRFX3, RFX3 and PROX1 on glioma cells. In vivo experiments were done to ascertain the impact of circRFX3 on glioma growth. Moreover, mechanism assays were conducted to investigate the molecular relation among circRFX3, RFX3, HNRNPK and PROX1.
resultsCircRFX3 was highly expressed in glioma cells. CircRFX3 knockdown led to the suppression of glioma cell and tumor growth. CircRFX3 overexpression resulted in the opposite outcomes. Mechanism analyses suggested that circRFX3 recruited HNRNPK to enhance RFX3 mRNA stability, thereby facilitating glioma cell malignant behaviors. RFX3 was also unveiled to affect glioma cells via stimulating PROX1 transcription.
conclusionCircRFX3, as a tumor promoter, could recruit HNRNPK to stabilize RFX3 mRNA in glioma cells. Additionally, RFX3 could promote PROX1 transcription to promote glioma progression.
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Registered trials
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