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• W4296886614 endingPage "120993" @default.
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• W4296886614 abstract "Breast cancer is one of the most common malignant tumors with a high incidence and leading cancer-related death in women worldwide. MiR-205 plays a crucial role in breast cancer initiation and progression. Here, we identified the relationship between miR-205 and lymphoid specific helicase and confirmed the significance of the miR-205/lymphoid specific helicase (miR-205/HELLS) axis.Data from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were analyzed to investigate the expression level of miR-205 and HELLS in breast cancer. The TargetScan, Starbase and miRWalk databases were used to predict the candidate target genes of miR-205. Proliferation and migration abilities were examined using cell counting kit-8 assay, colony formation assays, transwell assay and wound-healing assay. Dual-luciferase reporter assay was utilized to confirm the binding of miR-205 and HELLS. Quantitative RT-PCR, western blot assays or immunohistochemistry were conducted to detect the expression level of genes in breast cancer cells or tissues. Mice xenograft models were constructed to explore the function of miR-205 and HELLS in vivo.Overexpressed miR-205 alleviated cancer cell proliferation and migration and influenced patients' prognosis by negatively regulating the HELLS gene. Consistently, animal experiments revealed that both overexpressing miR-205 and knocking down HELLS exhibited significant tumor growth inhibition in vivo.Our study demonstrated that miR-205 targets HELLS to regulate tumor progression. MiR-205 and HELLS could be considered a novel diagnosis and therapeutic molecular marker of breast cancer." @default.
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• W4296886614 date "2022-11-01" @default.
• W4296886614 modified "2023-09-27" @default.
• W4296886614 title "Regulation of antitumor miR-205 targets oncogenes: Direct regulation of lymphoid specific helicase and its clinical significance" @default.
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• W4296886614 doi "https://doi.org/10.1016/j.lfs.2022.120993" @default.
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