ArticleCancer gene therapy2023
m6A-modified circABCC4 promotes stemness and metastasis of prostate cancer by recruiting IGF2BP2 to increase stability of CCAR1.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 24 citations in OpenAlex.
- N6-methyladenosine-modified circLPAR3 drives docetaxel resistance in prostate cancer by suppressing ferroptosis through the PCBP2/CHAC1 axis.Genes & diseases · 2026Article
- Hsa_circ_0030568 Promotes the Proliferation and Migration of Prostate Cancer CellsCombinatorial chemistry & high throughput screening · 2026Article
- Functions and mechanisms of circular RNAs in cancer stem cells and therapy resistance.Frontiers in cell and developmental biology · 2026Review
- RNA methylation in urological cancers: regulatory logic, biological functions, and clinical relevance.Frontiers in immunology · 2026Review
- Serine/Threonine Kinase 33 as a Novel Target of Bufalin in Treatment of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Circ_0000847 promotes the migration, invasion, and EMT process in colorectal cancer through binding to IGF2BP2 to enhance IGF2 mRNA stability.Medical oncology (Northwood, London, England) · 2025Article
- Emerging implications of N6-methyladenosine in prostate cancer progression and treatment.Cell death discovery · 2025Review
- Regulatory roles of circular RNAs in Wnt and other oncogenic signaling pathways in breast cancer progression: a comprehensive review.European journal of medical research · 2025Review
- ALKBH5-mediated m6A regulates the alternative splicing events of SRSF10 in ovarian cancer.Cancer gene therapy · 2025Article
- IGF2BP2: an mCellular & molecular biology letters · 2025Review
- circDHX33 suppresses glycolysis, malignant proliferation, and metastasis in prostate cancer by interacting with RNA-binding protein IGF2BP2 to destabilize its protein.Cytotechnology · 2025Article
- Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).Molecular medicine reports · 2025Review
- CircAKT3 promotes prostate cancer proliferation and metastasis by enhancing the binding of RPS27A and RPL11.Molecular cancer · 2025Article
- Mechanisms and therapeutic implications of gene expression regulation by circRNA-protein interactions in cancer.Communications biology · 2025Review
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
- Genetic variants ofInternational journal of medical sciences · 2025Article
- Igniting Cold Tumors: Multi-Omics-Driven Strategies to Overcome Immune Evasion and Restore Immune Surveillance.Oncology research · 2025Review
- Genetic variants in canonical Wnt signaling pathway associated with pediatric immune thrombocytopenia.Blood advances · 2024Article
- Advanced approaches of the use of circRNAs as a replacement for cancer therapy.Non-coding RNA research · 2024Review
- Cross-talk between circRNAs and m6A modifications in solid tumors.Journal of translational medicine · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) is a malignant tumor of the urinary system. CircABCC4 has been demonstrated to promote the development of PCa; however, its regulatory mechanisms in PCa progression remain largely unknown. We found that circABCC4 was highly expressed in PCa tissues and cells, and elevated circABCC4 level indicated a poor overall survival of PCa patients. METTL3 overexpression increased circABCC4 expression via m6A modification in PCa cells. Functionally, knockdown of circABCC4 or METTL3 repressed PCa cell stemness, migration, and invasion in vitro and delayed PCa cancer growth and metastasis in vivo. circABCC4 knockdown-mediated inhibition in PCa cell stemness and metastasis could be counteracted by overexpression of wild-type circABCC4 with m6A sites. Mechanistically, circABCC4 recruited IGF2BP2 protein to CCAR1 mRNA, thereby enhancing CCAR1 mRNA stability and subsequent activation of the Wnt/β-catenin pathway. Overexpression of CCAR1 counteracted the inhibitory effect of circABCC4 silencing on PCa cell stemness and metastasis. These results revealed that m6A-modified circABCC4 by METTL3 facilitated PCa cell stemness and metastasis by interacting with IGF2BP2 to increase the stability and expression of CCAR and subsequent expression of Wnt/β-catenin target genes. Our findings suggest circABCC4 as a promising therapeutic target for PCa.
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