Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
[Salidroside Inhibits the Proliferation of Gastric Cancer Cells by Regulating the miR-1343-3p/SOX18 Signaling Axis].
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Zhang Zhendong, Cao Xiaolan, Hou Xinrui, Cao Mingyuan, DU Yuxin, Zhang Jie, Sun Yanan, Wang Xiaoping
Аннотация
OBJECTIVE: To investigate the molecular mechanism by which salidroside inhibits the proliferation of gastric cancer (GC) cells through upregulation of miR-1343-3p.
METHODS: RNA databases were used to screen for mRNAs associated with tumor proliferation and with miR-1343-3p, and exhibiting significant changes in their expression levels after salidroside treatment of human GC cells. Gene matching and immunoprecipitation of RNA-binding proteins were conducted to analyze the association between miR-1343-3p and SOX18. Immunocytochemistry was performed to determine the localization of SOX18 protein. The effect of salidroside on the proliferation of human GC cells (MGC-803 and AGS) was determined by CCK-8 assay. Human GC cells were divided into a blank control group and low- and high-dose salidroside groups. The expression of miR-1343-3p and SOX18 mRNA was measured by real-time quantitative fluorescence PCR (qPCR). The protein expression of SOX18 was measured by Western blot. GC cells were co-transfected with miR-1343-3p mimic and miR-1343-3p inhibitor, respectively, via LipofectamineTM 2000 liposomes. The expression of miR-1343-3p and SOX18 mRNA was measured by qPCR, and the protein expression of SOX18 was measured by Western blot.
RESULTS: Through bioinformatic analysis, SOX18 was identified as a downstream target of miR-1343-3p. Gene alignment confirmed the presence of specific binding sites between the two genes, and immunoprecipitation of RNA-binding proteins validated the targeting relationship between them (P < 0.05). Immunocytochemistry demonstrated the nuclear localization of SOX18 protein. CCK-8 assay findings demonstrated that salidroside significantly inhibited the proliferation of GC cells in a time- and dose-dependent manner. Compared with the blank control group, salidroside-treated GC cells showed decreased expression of both SOX18 mRNA and protein (P < 0.05) and an increased miR-1343-3p expression (P < 0.05). Compared with the control group, GC cells in the miR-1343-3p mimic group exhibited increased expression of miR-1343-3p and decreased expression of SOX18 mRNA and protein. In contrast, GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein (all P < 0.05).
CONCLUSION: Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.
METHODS: RNA databases were used to screen for mRNAs associated with tumor proliferation and with miR-1343-3p, and exhibiting significant changes in their expression levels after salidroside treatment of human GC cells. Gene matching and immunoprecipitation of RNA-binding proteins were conducted to analyze the association between miR-1343-3p and SOX18. Immunocytochemistry was performed to determine the localization of SOX18 protein. The effect of salidroside on the proliferation of human GC cells (MGC-803 and AGS) was determined by CCK-8 assay. Human GC cells were divided into a blank control group and low- and high-dose salidroside groups. The expression of miR-1343-3p and SOX18 mRNA was measured by real-time quantitative fluorescence PCR (qPCR). The protein expression of SOX18 was measured by Western blot. GC cells were co-transfected with miR-1343-3p mimic and miR-1343-3p inhibitor, respectively, via LipofectamineTM 2000 liposomes. The expression of miR-1343-3p and SOX18 mRNA was measured by qPCR, and the protein expression of SOX18 was measured by Western blot.
RESULTS: Through bioinformatic analysis, SOX18 was identified as a downstream target of miR-1343-3p. Gene alignment confirmed the presence of specific binding sites between the two genes, and immunoprecipitation of RNA-binding proteins validated the targeting relationship between them (P < 0.05). Immunocytochemistry demonstrated the nuclear localization of SOX18 protein. CCK-8 assay findings demonstrated that salidroside significantly inhibited the proliferation of GC cells in a time- and dose-dependent manner. Compared with the blank control group, salidroside-treated GC cells showed decreased expression of both SOX18 mRNA and protein (P < 0.05) and an increased miR-1343-3p expression (P < 0.05). Compared with the control group, GC cells in the miR-1343-3p mimic group exhibited increased expression of miR-1343-3p and decreased expression of SOX18 mRNA and protein. In contrast, GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein (all P < 0.05).
CONCLUSION: Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.