ArticleMolecular medicine (Cambridge, Mass.)2020
circCELSR1 facilitates ovarian cancer proliferation and metastasis by sponging miR-598 to activate BRD4 signals.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 30 citations in OpenAlex.
- BRD4 Induces Esophageal Squamous Cell Carcinoma Progression via the Wnt/β-catenin Pathway.Biochemical genetics · 2026Article
- Androgen-induced AR-BRD4 transcriptional regulatory complex promotes malignant proliferation of osteosarcoma cells.Cell death discovery · 2025Article
- Circular RNA-based liquid biopsy: a promising approach for monitoring drug resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Interplay of microRNAs and circRNAs in Epithelial Ovarian Cancer.Non-coding RNA · 2024Review
- Article
- Role of circular RNA as competing endogenous RNA in ovarian cancer (Review).International journal of molecular medicine · 2024Review
- Deregulated circRNAs in Epithelial Ovarian Cancer With Activity in PreclinicalCancer genomics & proteomics · 2024Review
- Methylation of BRD4 by PRMT1 regulates BRD4 phosphorylation and promotes ovarian cancer invasion.Cell death & disease · 2023Article
- High Expression Level of BRD4 Is Associated with a Poor Prognosis and Immune Infiltration in Esophageal Squamous Cell Carcinoma.Digestive diseases and sciences · 2023Article
- The emerging roles and potential applications of circular RNAs in ovarian cancer: a comprehensive review.Journal of cancer research and clinical oncology · 2023Review
- circANKRD17(has_circ_0007883) confers paclitaxel resistance of ovarian cancer via interacting with FUS to stabilize FOXR2.Molecular and cellular biochemistry · 2023Article
- The role of circRNAs in regulation of drug resistance in ovarian cancer.Frontiers in genetics · 2023Review
- Review
- Emerging role of circular RNAs in the pathogenesis of ovarian cancer.Cancer cell international · 2022Review
- Circ_0007580 knockdown strengthens the radiosensitivity of non-small cell lung cancer via the miR-598-dependent regulation of THBS2.Thoracic cancer · 2022Article
- The Anti-Tumor Efficacy of Verbascoside on Ovarian CancerFrontiers in oncology · 2022Article
- LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis.Cancer cell international · 2021Article
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8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOvarian cancer is one of the most common gynecologic cancers and has high mortality rate due to the lack of early diagnosis method and efficient therapeutic agents. circCELSR1 is up-regulated in ovarian cancer, but its role and mechanisms in ovarian cancer are unclear.
methodsGene expression of circCELSR1, miR-598 and BRD4 in ovarian cells was examined by qRT-PCR. Protein level was determined by Western blotting. Bioinformatic analysis and luciferase assay determined the molecular binding among circCELSR1, miR-598 and BRD4 3' UTR. Cell proliferation, migration, invasion and apoptosis were determined by colony formation, wound healing assay, transwell assay and flow cytometry analysis, respectively. An abdominal cavity metastasis nude mice model was used to determine the in vivo function of circCELSR1.
resultscircCELSR1 and BRD4 were promoted, but miR-598 was suppressed in various ovarian cancer cells. circCELSR1 bound to miR-598 and promoted expression of its downstream target BRD4. Knockdown of circCELSR1 suppressed proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), but promoted apoptosis in ovarian cancer cells, and these effects were reversed by miR-598 inhibition or BRD4 overexpression. circCELSR1 inhibition decreased the expression of BRD4 and its downstream proliferation/migration related genes by targeting miR-598. Furthermore, knockdown of circCELSR1 suppressed ovarian cancer growth and metastasis in nude mice.
conclusionKnockdown of circCELSR1 inhibited BRD4-mediated proliferation/migration related signaling via sponging miR-598, thereby repressing ovarian cancer progression. This study provides a new regulatory mechanism of ovarian cancer may facilitate the development of therapeutic agents for ovarian cancer.
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