Salidroside inhibits proliferation of gastric cancer cells by regulating the miR-1343-3p-OGDHL/PDHB glucose metabolic axis
HOU Xinrui
ZHANG Zhendong
CAO Mingyuan
DU Yuxin
WANG Xiaoping
Abstract：Objective To investigate the mechanism through which salidroside inhibits proliferation of gastric cancer(GC)cells focusing on glucose metabolic reprogramming pathways.Methods High-throughput sequencing combined with bioinformatics analysis was employed to identify the potential targets of salidroside in human GC MGC-803 cells.Liposome-mediated transfection experiments were carried out to validate the functional and mechanistic roles of these targets.CCK-8 and colony formation assays were used to assess the effects of salidroside on GC cell viability and clonogenic ability.qRT-PCR,Western blotting,and biochemical assay kits were used to analyze the regulatory effects of salidroside on the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway in GC cells.Results Bioinformatics analysis suggested that the tumor-suppressive factor miR-1343-3p negatively regulated the key glycolytic enzyme gene oxoglutarate dehydrogenase-like(OGDHL)in GC cells,and OGDHL and pyruvate dehydrogenase E1 subunit beta(PDHB)were both significantly upregulated in GC tissues,which was close by correlated with reduced survival rates of GC patients.In MGC-803 cells,salidroside treatment significantly enhanced the expression level of miR-1343-3p and downregulated OGDHL expression,resulting in disruption of the stability of PDHB,reduced pyruvate oxidative decarboxylation,and consequently decreased production of acetyl-CoA and ATP.Conclusion Salidroside inhibits GC cell proliferation possibly by regulating the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway,which provides new insights into its anti-tumor mechanisms and suggests new strategies for targeted therapy for GC.
Keywords：gastric cancerglucose metabolic reprogrammingsalidrosidemiR-1343-3poxoglutarate dehydrogenase-likepyruvate dehydrogenase E1 subunit beta
Publication Date：2025-06-20
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：14( 1226-1239 )