ArticleFrontiers in pharmacology2023
Chebulagic acid suppresses gastric cancer by inhibiting the AURKA/β-catenin/Wnt pathway.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Rambutan (Molecules (Basel, Switzerland) · 2026Article
- Chebulagic acid targets FBXO38 to enhance natural killer cell-mediated anti-tumor immunity in lung adenocarcinoma.Human cell · 2026Article
- Functional Roles and Mechanistic Insights of YEATS Domain Proteins in Digestive System Tumors.Digestive diseases and sciences · 2025Review
- Natural products targeting the MAPK signaling pathway: potential options for ulcerative colitis treatment.Frontiers in pharmacology · 2025Review
- Chebulagic acid ameliorates DSS-induced colitis in mice by improving oxidative stress, inflammation and the gut microbiota.American journal of translational research · 2025Article
- Comprehensive Review on Fruit ofMolecules (Basel, Switzerland) · 2024Review
- Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
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Abstract
Gastric cancer (GC) is a prevalent malignant neoplasm that poses a serious threat to human health. Overexpression of Aurora A (AURKA) is frequently associated with the self-renewal and tumorigenicity of various cancers. Chebulagic acid (CA) has been examined as a potential tumor suppressor based on its ability against numerous tumor biological activities. However, the possible mechanisms of CA inhibition of the progression of GC by mediating the AURKA/β-catenin/Wnt signaling pathway have not been investigated. The present study investigated the level of AURKA expression in GC. We further examined the effect of CA on cell proliferation, migration, and apoptosis in the MKN1 and NUGC3 GC cell lines, and its efficacy in suppressing tumor growth was assessed in tumor bearing mice model. We demonstrated that AURKA was highly expressed in GC and associated with poor prognosis. We demonstrated that treatment with CA significantly inhibited the proliferation and migration of GC cells and induced apoptosis. Compared to the vehicle group, CA treatment severely diminished the volume and weight and the metastasis of tumors. CA also inhibited the expression of AURKA and the AURKA/β-catenin/Wnt signaling pathway
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