LncRNA SNHG7 contributes to tumorigenesis and progression in breast cancer by interacting with miR-34a through EMT initiation and the Notch-1 pathway.

The long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) has been reported to be upregulated and contribute to carcinogenesis, progression and poor prognosis of many cancers. However, expression and function of SNHG7 in breast cancer remain unclear. Herein, we found that SNHG7 was significantly up-regulated in breast cancer tissues and cell lines. SNHG7 knockdown significantly inhibited MCF-7 cell proliferation and invasion, while SNHG7 overexpression dramatically promoted T47D cell proliferation and invasion. Xenograft experiments in vivo showed that SNHG7 knockdown significantly inhibited tumor growth in mice. In terms of mechanism, miR-34a was confirmed to be the target of SNHG7, and SNHG7 could sponge miR-34a to inhibit the expression of miR-34a. In vivo and in vitro experiments both showed that SNHG7 targeted miR-34a and promoted epithelial-to-mesenchymal transition (EMT) initiation and the Notch-1 pathway in breast cancer. In conclusion, SNHG7 promoted breast cancer tumorigenesis and progression by sponging miR-34a through EMT initiation and the Notch-1 pathway. These findings contribute to a better understanding of breast cancer pathogenesis and further provide the theoretical fundamental basis for treatment.