Salidroside Induces Apoptosis in Human Gastric Cancer Cells via the Downregulation of ENO1/PKM2/GLUT1 Expression
| Autor: | Ziying, Dai, Xuan, Zhang, Wuyan, Li, Junxia, Tang, Tingting, Pan, Chenru, Ma, Quanlin, Guan |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Glucose Transporter Type 1
Mice Inbred BALB C Thyroid Hormones Plant Extracts Tumor Suppressor Proteins Down-Regulation Membrane Proteins Mice Nude Apoptosis Antineoplastic Agents Phytogenic Xenograft Model Antitumor Assays DNA-Binding Proteins Glucosides Phenols Stomach Neoplasms Cell Line Tumor Phosphopyruvate Hydratase Biomarkers Tumor Animals Humans Rhodiola Carrier Proteins Glycolysis Cell Proliferation Phytotherapy |
| Zdroj: | Biologicalpharmaceutical bulletin. 44(11) |
| ISSN: | 1347-5215 |
| Popis: | Salidroside is reported to have a wide range of pharmacological properties and has been proven to play a key anti-cancer effect. This study investigated the effects of purified salidroside, an ingredient of Rhodiola rosea, on the proliferation of two human gastric cancer cell lines and further investigating its possible molecular mechanisms. We verified that salidroside exerts a dose-dependent inhibitory effect on the proliferation of SGC-7901 and MKN-45 human gastric cancer cells. Moreover, salidroside can induce cell apoptosis, which was accompanied by an increase in nuclear fragmentation. In addition, salidroside inhibited glycolysis, as evidenced by the reduced expression levels of the glycolysis-related enzymes pyruvate kinase isoenzyme M2 (PKM2), enolase 1 (ENO1) and glucose transporter 1 (GLUT1), which could play important roles in the metabolism of gastric cancer cells. Further investigation showed that salidroside exerted potent anti-proliferative effects by inhibiting glycolysis in human gastric cancer cells in vitro. In vivo, xenograft tumors treated with salidroside were significantly smaller than those in the control animals. Therefore, salidroside could be a promising therapeutic prospect in the treatment of gastric cancer. |
| Databáze: | OpenAIRE |
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