ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Metabolism
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1651857
Salidroside Suppresses Gastric Cancer Progression via miR-1343-3p-Mediated Repression of ACOT11 and Disruption of Fatty Acid Metabolism
Provisionally accepted
- Xizang Minzu University, Xianyang, China
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Objective Salidroside, a bioactive compound derived from Rhodiola, has been demonstrated to upregulate the tumor suppressor miR-1343-3p, leading to suppression of gastric cancer growth. However, the precise molecular mechanisms underlying salidroside-mediated regulation of lipid metabolism via miR-1343-3p and its downstream mRNA targets remain poorly understood. Methods The interaction between miR-1343-3p and ACOT11 was evaluated through Pearson correlation analysis, sequence-based binding site alignment, and RNA immunoprecipitation (RIP) assays. The effects of salidroside treatment on cell proliferation, gene and protein expression, downstream metabolites, and energy production were assessed through a series of in vitro and in vivo experiments, including the CCK-8 assay, colony formation assay, RT-qPCR, Western blot, ELISA, cell transfection, and xenograft tumor models. Results The expression of miR-1343-3p is negatively correlated with ACOT11 mRNA, which is closely associated with lipid metabolism. Salidroside significantly inhibits the proliferation of gastric cancer cells in a dose-dependent manner. Compared to untreated controls, salidroside-treated gastric cancer cells showed decreased ACOT11 mRNA/protein expression but increased miR-1343-3p levels. This was accompanied by elevated substrate fatty acyl-CoA concentrations with concurrent reductions in acetyl-CoA, FFA, and ATP. ACOT11 is a downstream target of miR-1343-3p, up-regulating miR-1343-3p expression reduces ACOT11 expression, while down-regulating miR-1343-3p expression increases ACOT11 expression. In vivo, salidroside significantly inhibited tumor growth in gastric cancer xenograft models. Conclusions We demonstrate that salidroside exerts anti-proliferative effects in gastric cancer by targeting the miR-1343-3p/ACOT11/FFA lipid metabolism signaling pathway, disrupting cancer cell energy production. These regulatory factors hold promise as novel therapeutic targets for gastric cancer.
Keywords: gastric cancer, Salidroside, Lipid Metabolism, miR-1343-3p, ACOT11
Received: 22 Jun 2025; Accepted: 15 Aug 2025.
Copyright: © 2025 Zhang, Cao, Du, Wang, Hou and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Xiaoping Wang, Xizang Minzu University, Xianyang, China
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