ArticleThoracic cancer2024
Exosome-transported circ_0001955 as a potent driver of breast cancer by regulating the miR-708-5p/PGK1 axis.
Article in Thoracic cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Circular RNAs: key regulators of paclitaxel sensitivity and resistance in cancer.European journal of medical research · 2025Review
- Exosomal circRNAs: key modulators in breast cancer progression.Cell death discovery · 2025Review
- Exosome-transported circ_0001955 as a potent driver of breast cancer by regulating the miR-708-5p/PGK1 axis.Thoracic cancer · 2024Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing evidence shows that exosome-mediated delivery of circular RNA (circRNA) is implicated in breast cancer progression. This study aimed to elucidate the role of exosome-transported circ_0001955 in breast cancer.
methodsThe expression of circ_0001955, miR-708-5p, and phosphoglycerate kinase 1 (PGK1) messenger RNA (mRNA) was detected by quantitative real-time polymerase chain reaction (qRT-PCR); the protein levels of PGK1 and hexokinase 2 (HK2) were detected by western blot (WB). 5'-Ethynyl-2'-deoxyuridine (EdU) and colony formation assay were used to determine cell proliferation. Glycolytic metabolism was analyzed by corresponding kits to detect the associated indicators. The role of circ_0001955 in vivo was studied by establishing animal models. The potential binding relationship between miR-708-5p and circ_0001955 or PGK1 was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
resultsCirc_0001955 was highly expressed in breast cancer tissues and cell lines, as well as in exosomes from breast cancer cell lines. The deficiency of circ_0001955 blocked proliferation, decreased the IC50 value of paclitaxel (PTX), and blocked glycolysis in MCF-7 and MDA-MB-231 cells. Circ_0001955 knockdown also inhibited tumor growth in vivo. Circ_0001955 directly combined with miR-708-5p, and the miR-708-5p inhibitor reversed the effects of sh-circ_0001955. PGK1 was a target of miR-708-5p, and circ_0001955 indirectly promoted PGK1 expression by binding to miR-708-5p. PGK1 overexpression abolished the function of miR-708-5p in breast cancer.
conclusionExosomal circ_0001955 excreted from breast cancer cells facilitated proliferation and glycolysis and enhanced the IC50 value of PTX in breast cancer cells by sponging miR-708-5p to upregulate PGK1.
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