Toosendanin induces apoptosis of MKN-45 human gastric cancer cells partly through miR-23a-3p-mediated downregulation ofBCL2

Toosendanin (TSN) is a tetracyclic triterpenoid extracted fromMelia toosendanSieb, et Zucc, which primarily grows in specific areas of China. Although toosendanin (TSN) exerts antitumoral effects on various human cancer cells, its influence on gastric cancer (GC) is remains to be elucidated. MicroRNAs (miRNAs/miRs) serve crucial roles in apoptosis and proliferation of cancer cells. miR-23a-3p has been shown to be associated with human GC; however, the specific function of miR-23a-3p in GC remains unclear. Therefore, the present study aimed to elucidate the role of miR-23a-3p in the regulation of GC cell proliferation and apoptosis inducedin vitroby TSN treatment. Subsequently, apoptosis-related genes expression levels were quantified by reverse transcription-quantitative PCR and western blot analysis, respectively, and the target relationship between miR-23a-3p andBCL2was determined by luciferase reporter gene analysis. Additionally, cell proliferation and apoptosis experiments were carried out. The results indicated that TSN inhibited proliferation and induced apoptosis in MKN-45 cells. Moreover, it upregulated the expression of miR-23a-3p. B-cell lymphoma-2 (BCL2) was identified as a potential target gene of miR-23a-3p, which was demonstrated to bind to the 3 '-untranslated region ofBCL2mRNA, as detected by the luciferase reporter assay. Further studies revealed thatBCL2expression was downregulated following overexpression of miR-23a-3p. In addition, the overexpression of the miR-23a-3p inhibited proliferation, induced G(1)arrest and increased apoptosis in MKN-45 cells. The results of the present study demonstrated that miR-23a-3p inhibited proliferation and induced apoptosis of GC cells, which may be attributable to its direct targeting ofBCL2. These results may provide a novel insight into the apoptosis of GC cells, and may lead to investigations into the mechanisms of the effects of TSN.