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• W2951094725 abstract "Recently, microRNA (miR)‑628 was identified as a potential biomarker for several types of cancer, including prostate cancer (PCa). The aim of the present study was to investigate miR‑628 expression and its underlying mechanism in PCa cell proliferation and invasion and the fibroblast growth factor receptor 2 (FGFR2) signaling pathway. The serum expression levels of miR‑628, prostate‑specific antigen, fibroblast growth factor 1, and FGFR2 were examined in patients with PCa. The relative expression levels of miR‑628 and FGFR2 were determined by reverse transcription‑quantitative polymerase chain reaction in PCa cells following transfection with miR‑628‑5p mimic or inhibitor. In addition, the protein expression level of FGFR2 was examined by western blot analysis following transfection with miR‑628‑5p mimic or inhibitor. Following bioinformatics analysis, dual‑luciferase reporter assay was used to confirm the direct interaction between miR‑628 and FGFR2. The current study demonstrated that the protein expression level of FGFR2 decreased following transfection with miR‑628‑5p mimic and increased following transfection with miR‑628‑5p inhibitor. Similarly, the proliferation and invasion of PCa cells were significantly enhanced following transfection with miR‑628‑5p inhibitor. By contrast, the proliferation and invasion of PCa cells were significantly inhibited following transfection with miR‑628 mimic. Therefore, downregulating the expression level of miR‑628 may increase the expression level of FGF in PCa, thereby promoting tumor proliferation and invasion. In conclusion, the FGF signaling pathway may be involved in promoting PCa cell proliferation and invasion. miR‑628 may be a potential therapeutic target for patients with PCa." @default.
• W2951094725 created "2019-06-27" @default.
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• W2951094725 date "2019-06-18" @default.
• W2951094725 modified "2023-10-04" @default.
• W2951094725 title "miR‑628 reduces prostate cancer proliferation and invasion via the FGFR2 signaling pathway" @default.
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• W2951094725 doi "https://doi.org/10.3892/etm.2019.7682" @default.
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