ArticleFrontiers in oncology2025
Salidroside suppresses gastric cancer progression via miR-1343-3p-mediated repression of ACOT11 and disruption of fatty acid metabolism.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Salidroside represses ovarian cancer progression by targeting FSP1-dependent ferroptosis.Journal of ovarian research · 2026Article
- Acyl-CoA thioesterases and their derived lipid mediators: linking Acyl-CoA metabolic reprogramming to the tumor microenvironment.Frontiers in immunology · 2026Review
- miR-1343-3p regulating OGDHL/PDHB-pyruvate glucose metabolic reprogramming against gastric cancer cell proliferation.Discover oncology · 2025Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
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 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. 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.
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