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Updated: Oct 5, 2025

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
CircPDE7B/miR-661 axis accelerates the progression of human keloid fibroblasts by upregulating fibroblast growth
Fenglian Wu1, Hongbin He1, Yanxin Chen2
1Department of Plastic Surgery, The First Hospital of Qinhuangdao, No. 258, Wenhua Road, Qinhuangdao, 066000, Hebei, China.
Abstract:
Circular RNAs (circRNAs) are implicated in keloidogenesis and development. We aimed to investigate the role of a new identified phosphodiesterase 7B-derived circRNA (hsa_circ_0002198; henceforth named as PDE7B) in human keloid fibroblasts (HKFs) and to further confirm its mechanism via competing endogenous RNA (ceRNA) network. Transcriptional and translational levels of circPDE7B, microRNA (miR)-661, fibroblast growth factor 2 (FGF2), cleaved caspase3, B-cell lymphoma (bcl)-2, and bcl-2-associated X protein (bax) were detected by real-time quantitative PCR and western blotting. Relationship among circPDE7B, miR-661, and FGF2 was confirmed by bioinformatics algorithm, dual-luciferase reporter assay, RNA immunoprecipitation, RNA pull-down assay, and Spearman's rank correlation analysis. Cell progression was measured by cell counting kit-8 assay, 5-ethynyl-2-deoxyuridine assay, transwell assays, and flow cytometry. Expression of circPDE7B was upregulated in human keloid tissues and HKFs, accompanied with miR-661 downregulation and FGF2 upregulation. High circPDE7B accelerated proliferation, migration, and invasion, and inhibited apoptosis. These effects were paralleled with increased bcl-2 and decreased cleaved caspase3 and bax. Moreover, low circPDE7B played opposite effects to high circPDE7B. Restoring miR-661 could suppress HKFs progression, while blocking miR-661 could facilitate that. Notably, miR-661 was directly sponged by circPDE7B and then directly governed FGF2 gene expression. Deleting miR-661 and re-expressing FGF2 both abrogated the suppression of circPDE7B knockdown in HKFs progression. In conclusion, circPDE7B might contribute to HKFs progression via functioning as ceRNA for miR-661, suggesting a novel circPDE7B/miR-661/FGF2 pathway underlying keloid formation and treatment.
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