Abstract
Accumulating evidence suggests that long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SHNG3) plays crucial roles in the initiation and progression of various types of malignant cancers. Yet, the role played by SNHG3 in breast cancer as well as the associated mechanisms remain largely unclear. The expression of SNHG3 was detected in breast cancer tissues and cell lines by reverse‑transcription quantitative PCR (RT‑qPCR). Cell proliferation, colony formation, cell cycle distribution, migration and invasion abilities were detected by Cell Counting Kit‑8, colony formation assay, flow cytometry, wound‑healing and Matrigel invasion assays, respectively. The regulatory relationships between SNHG3 and miR‑326 were explored by luciferase reporter assay. A nude mouse model was established to investigate the effect of SNHG3 in vivo. The results showed an upregulation of SNHG3 in breast cancer tissues and cell lines. Loss‑of‑function assays revealed significant suppression of breast cancer behaviors such as: Abilities to proliferate, form colonies, migrate and invade in vitro coupled with a delayed growth of tumors in vivo when SNHG3 was knocked down. Mechanically, it was shown that SNHG3 served as a competing endogenous RNA (ceRNA) of miR‑326 that in turn is a tumor suppressor in this cancer. The correlation between the expression of SNHG3 and miR‑326 was found to be strongly negative in these samples. Additionally, we found that inhibition of SNHG3 caused a partially reversal in the inhibition exerted by miR‑326 on the ability of these cells to proliferate, form colonies, migrate and invade. Collectively, these findings suggest the functioning of SNHG3 as a ceRNA to enhance the ability of breast cancer cells to proliferate and metastasize to putatively serve as a new target to explore therapeutic intervention of this malignancy.