ArticleHistology and histopathology2023
The circCDK17/miR-122-5p/ASF1B axis regulates the progression of cervical cancer.
Article in Histology and histopathology, 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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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- LncRNA SNHG11 expression in acute myeloid leukemia patients and its relationship with the biology of acute myeloid leukemia cells.Clinical and experimental medicine · 2025Article
- Transforming Properties of E6/E7 Oncogenes from Beta-2 HPV80 in Primary Human Fibroblasts.International journal of molecular sciences · 2025Article
- Insights into the structural and functional activities of forgotten Kinases: PCTAIREs CDKs.Molecular cancer · 2024Review
- The potential role and mechanism of circRNA/miRNA axis in cholesterol synthesis.International journal of biological sciences · 2023Review
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCervical cancer (CC) ranks fourth in terms of incidence and fourth in mortality overall in women worldwide. Circular RNAs (circRNAs) have been shown to be involved in the development of CC. However, the function of circRNA cyclin dependent kinase 17 (circCDK17, hsa_circ_0002762) in CC pathogenesis has not been studied.
methodsQuantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of related genes. MTT, thymidine analog 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays were designed to analyze cell proliferation, cell cycle progression, migration and invasion, respectively. Western blot was utilized to examine the protein levels of Cyclin D1, E-cadherin and Vimentin. The relationship between miR-122-5p and circCDK17 or ASF1B was verified by dual-luciferase reporter assay. The xenograft model was established to study the role of circCDK17 in vivo.
resultsCircCDK17 and anti-silencing function 1B histone chaperone (ASF1B) were highly expressed in CC tissues and cells. Silencing circCDK17 reduced the proliferation, migration and invasion of CC cells. MiR-122-5p was a target of circCDK17. Silencing circCDK17 inhibited the malignant behaviors of CC cells by releasing miR-122-5p. Moreover, ASF1B was a target of miR-122-5p. Overexpression of ASF1B partially restored the inhibitory effects of circCDK17 silencing on cell proliferation, migration and invasion. Animal experiments confirmed the anti-tumor effect of circCDK17 knockdown in vivo.
conclusionOur study demonstrates that circCDK17 regulates the expression of ASF1B by miR-122-5p competition and thus promotes the development of CC, providing a novel targeted therapy for CC.
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