ArticleCell death & disease2022
UPF1/circRPPH1/ATF3 feedback loop promotes the malignant phenotype and stemness of GSCs.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- CircRPPH1 promotes hepatocellular carcinoma progression through inhibiting PPARα transcription and accelerating its ubiquitination and degradation.Cellular and molecular life sciences : CMLS · 2026Article
- Review
- Functions and mechanisms of circular RNAs in cancer stem cells and therapy resistance.Frontiers in cell and developmental biology · 2026Review
- The MCU-MECOM Axis Orchestrates Glioblastoma Progression by Remodeling Mitochondrial Dynamics and Quality Control via MAMs.International journal of biological sciences · 2026Article
- UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma.Frontiers in immunology · 2026Article
- Role of Colony Stimulating Factor 1 (CSF-1) and Its Receptor CSF1R: Macrophage Repolarization for Glioblastoma Treatment.ACS pharmacology & translational science · 2025Review
- Single-cell transcriptomics reveals hypoxia-driven iCAF_PLAU is associated with stemness and immunosuppression in anorectal malignant melanoma.Journal of gastroenterology · 2025Article
- PDK1-dependent metabolic reprogramming regulates stemness and tumorigenicity of osteosarcoma stem cells through ATF3.Cell death & disease · 2025Article
- CircMAN1A2 Levels Determine GBM Susceptibility to TMZ in a Pathway Involving TEP1- and KEAP1-Mediated NRF2 Degradation Leading to Ferroptosis.CNS neuroscience & therapeutics · 2025Article
- Circular RNAs in cancer stem cells: Insights into their roles and mechanisms (Review).International journal of molecular medicine · 2025Review
- Mechanisms and therapeutic implications of gene expression regulation by circRNA-protein interactions in cancer.Communications biology · 2025Review
- Old players and new insights: unraveling the role of RNA-binding proteins in brain tumors.Theranostics · 2025Review
- Regulatory role of circular RNAs in the development of therapeutic resistance in the glioma: A double-edged sword.Iranian journal of basic medical sciences · 2025Review
- CircMAPK1 induces cell pyroptosis in sepsis-induced lung injury by mediating KDM2B mRNA decay to epigenetically regulate WNK1.Molecular medicine (Cambridge, Mass.) · 2024Article
- Glioblastoma stem cells deliver ABCB4 transcribed by ATF3 via exosomes conferring glioblastoma resistance to temozolomide.Cell death & disease · 2024Article
- The Glioblastoma CircularRNAome.International journal of molecular sciences · 2023Review
- Review
- C-Fos-activated circRPPH1 contributes to glioma stemness.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- CircLPAR1 Promotes Neuroinflammation and Oxidative Stress in APP/PS1 Mice by Inhibiting SIRT1/Nrf-2/HO-1 Axis Through Destabilizing GDF-15 mRNA.Molecular neurobiology · 2023Article
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most lethal type of craniocerebral gliomas. Glioma stem cells (GSCs) are fundamental reasons for the malignancy and recurrence of GBM. Revealing the critical mechanism within GSCs' self-renewal ability is essential. Our study found a novel circular RNA (circRPPH1) that was up-regulated in GSCs and correlated with poor survival. The effect of circRPPH1 on the malignant phenotype and self-renewal of GSCs was detected in vitro and in vivo. Mechanistically, UPF1 can bind to circRPPH1 and maintain its stability. Therefore, more existing circRPPH1 can interact with transcription factor ATF3 to further transcribe UPF1 and Nestin expression. It formed a feedback loop to keep a stable stream for stemness biomarker Nestin to strengthen tumorigenesis of GSCs continually. Besides, ATF3 can activate the TGF-β signaling to drive GSCs for tumorigenesis. Knocking down the expression of circRPPH1 significantly inhibited the proliferation and clonogenicity of GSCs both in vitro and in vivo. The overexpression of circRPPH1 enhanced the self-renewal of GSCs. Our findings suggest that UPF1/circRPPH1/ATF3 maintains the potential self-renewal of GSCs through interacting with RNA-binding protein and activating the TGF-β signal pathway. Breaking the feedback loop against self-renewing GSCs may represent a novel therapeutic target in GBM treatment.
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Registered trials
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.