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| The Mechanism of miR-141-3p Targeting CDC25B to Regulate VEGF Pathway on Angiogenesis of Triple-Negative Breast Cancer |
| CHEN Yanzhi |
| Jiangxi Medical College, Jiangxi Shangrao 333400, China |
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Abstract Objective: To investigate the exact function and mechanism of CDC25B in TNBC angiogenesis.Methods: Bioinformatics database was used to analyze the expressions of CDC25B and its upstream regulatory molecule miR-141-3p in TNBC tumor tissues, and qRT-PCR was used to analyze the expressions of CDC25B and miR-141-3p in TNBC cell lines. The proliferation and angiogenesis capacity of HUVEC cells were analyzed by CCK-8 and angiogenesis assay, and the expressions of VEGFA, VEGFR-2 and VEGFR-3 proteins were detected by Western blot. Dual luciferase reporter assay was used to explore the specific interaction between CDC25B and miR-141-3p.Results: It was found that CDC25B was up-regulated in TNBC, and its high expression could activate the VEGF signaling pathway, and the silencing of CDC25B significantly inhibited the proliferation and angiogenesis of HUVEC cells, and decreased the expression of VEGFA, VEGFR-2 and VEGFR-3 proteins. In addition, the expression of miR-141-3p was down-regulated in TNBC, which could target the inhibition of CDC25B expression. Overexpression of CDC25B reversed the inhibitory effect of miR-141-3p overexpression on proliferation and angiogenesis of HUVEC cells.Conclusion: miR-141-3p targets CDC25B to inhibit VEGF pathway and inhibit TNBC angiogenesis, and we provide theoretical basis for the possibility of miR-141-3p/CDC25B/VEGF pathway as a new choice for TNBC anti-angiogenesis therapy.
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2023, Vol. 29 
