Abstract

Breast cancer (BC) is a highly prevalent aggressive malignancy in women worldwide, and the search for key targets in its pathogenesis is a focus of research. Long non-coding RNAs (lncRNAs) play an important role in many cancers, including breast cancer. This study aimed to investigate the role of lncRNA SNHG9 in BC. The expression of SNHG9 in BC cells was found to be higher than that of human mammary epithelium. SNHG9 was found to inhibit the proliferation, migration, and invasion of cells and promote apoptosis. It was also found that SNHG9 regulates the miR-326/Wnt5a/β-catenin axis to promote the development of BC. Dual luciferase reporter and RNA pull-down assays confirmed the interaction between SNHG9, Wnt5a, and miR-326. Western blot analysis indicated that the expression of Wnt5a, β-catenin, c-myc, and cyclin D1 decreased significantly after the silencing of SNHG9 and the overexpression of miR-326. On the contrary, Wnt5a, β-catenin, c-myc, and cyclin D1 proteins were significantly up-regulated after inhibiting miR-326 expression. These findings suggest that SNHG9 is a promising target for BC therapy.

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