Sodium Selenite Regulates the Proliferation and Apoptosis of Gastric Cancer Cells by Suppressing the Expression of LncRNA HOXB-AS1.

Gastric carcinoma has a high incidence, accounting for approximately 6% of all cancers worldwide. The in vivo antitumor effect of sodium selenite on gastric carcinoma has been demonstrated. This study therefore aimed to further explore its targets in gastric cancer in vitro and elucidate its mechanism of action. The effects of inorganic sodium selenite (NaSeO) on apoptosis, proliferation, and invasion of gastric cancer cells were investigated, and the interaction between NaSeO and expression of long noncoding RNA homeobox B cluster antisense RNA 1 (HOXB-AS1) was investigated to elucidate the specific mechanism of action of selenium on gastric cancer cell proliferation through regulation of HOXB-AS1. NaSeO downregulated the expression of HOXB-AS1 in the human gastric cancer (HGC) cell lines, HGC-27, NCI-N87, and KATO III cells, while inhibiting their proliferation and invasion and inducing apoptosis. The upregulation of HOXB-AS1 produced the opposite results. NaSeO was used to stimulate HGC-27 cells, which caused HOXB-AS1 overexpression. The cell counting kit-8 (CCK-8) assay revealed a decrease in cell proliferation, while western blotting, flow cytometry, and transwell migration assays showed the expression of apoptosis-related (Bad, Bcl-2, and cleaved-caspase-3) and invasion-related (MMP2, E-cadherin, and N-cadherin) proteins, indicating increased apoptosis and decreased invasion. We therefore conclude that NaSeO inhibits the malignant progression of gastric cancer by downregulating the expression of HOXB-AS1 and thus could be used as a potential drug for its treatment.