ArticleMolecular biotechnology2024
CircPRRC2C Promotes the Oncogenic Phenotypes of Laryngeal Squamous Cell Carcinoma Cells via MiR-136-5p/HOXD11 Axis.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- DNMT1 promotes the malignant progression of colorectal cancer by silencing HOXD11 via promoter hypermethylation.Discover oncology · 2026Article
- Hsa_circYARS interacts with miR-29a-3p to up-regulate IREB2 and promote laryngeal squamous cell carcinoma progression.Discover oncology · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of circular RNAs (circRNAs) in laryngeal squamous cell carcinoma (LSCC) carcinogenesis has gradually been proposed. Herein, we aimed to explore the function and mechanism of circPRRC2C in LSCC. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for detecting the content of genes and proteins. In vitro experiments were conducted using 5-ethynyl-2'-deoxyuridine, colony formation, flow cytometry, and transwell assays. The binding between miR-136-5p and circPRRC2C or Homeobox D11 (HOXD11) was confirmed by using the dual-luciferase reporter assay. The murine xenograft model was established for in vivo analysis. The commercial kit was used for exosome separation. CircPRRC2C is a stable circRNA, and was highly expressed in LSCC tissues and cell lines. Functionally, circPRRC2C deficiency impaired LSCC cell proliferation, migration and invasion but induced cell apoptosis in vitro and impeded tumor growth in vivo, however, circPRRC2C overexpression showed the exact opposite effects. Mechanistically, circPRRC2C directly targeted miR-136-5p, which showed inhibitory effects on the growth and mobility of LSCC cells. Meanwhile, miR-136-5p directly targeted HOXD11, and circPRRC2C/miR-136-5p/HOXD11 formed a feedback loop in LSCC cells. Further rescue assays exhibited that circPRRC2C exerted its effects by miR-136-5p/HOXD11 axis. In addition, circPRRC2C was stably packaged into exosomes and showed potential diagnostic value for LSCC. CircPRRC2C acted as an oncogene to promote LSCC cell oncogenic phenotypes via miR-136-5p/HOXD11 axis, besides, circPRRC2C was stably packaged into exosomes, indicating the potential application of circPRRC2C-targeting agents in the treatment in LSCC.
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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.