Abstract
The long-non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) is a known cause of tumorigenesis. Nevertheless, it's yet unclear how lncRNA SNHG1 influences breast cancer. Herein, we explored the mechanisms through which SNHG1 modulates breast cancer tumor progression. Our findings demonstrated that SNHG1 is significantly upregulated in breast cancer tissues and cells. High SNHG1 levels were closely linked to reduced survival rates in breast cancer patients. SNHG1 silencing has been shown to inhibit the proliferative, migratory, and invasive activity of breast cancer cells. Moreover, SNHG1 silencing enhanced cisplatin (DDP) sensitivity of these cells through improving DDP-induced cell apoptosis. Mechanistically, SNHG1 was found to interact with enhancer of zeste homolog 2 (EZH2), recruiting EZH2 to trigger trimethylation of histone H3 lysine 27 (H3K27me3), thus epigenetically inhibiting miR-381 transcription in these cells. Overexpression of miR-381 inhibited tumor progression and sensitized cells to the chemotherapeutic reagent DDP. More importantly, rescue experiments demonstrated that miR-381 inhibition could inverse the tumor-suppressive effect of SNHG1 silencing in breast cancer. In summary, SNHG1 silencing suppressed tumor progression and overcame breast cancer cell DDP resistance via the epigenetic suppression of miR-381 expression. Our study revealed that SNHG1 served as a novel therapeutic target for breast cancer chemoresistance.