ArticleFrontiers in oncology2022
Glaucocalyxin A Inhibits the Malignant Progression of Epithelial Ovarian Cancer by Affecting the MicroRNA-374b-5p/HMGB3/Wnt-β-Catenin Pathway Axis.
Article in Frontiers in oncology, 2022. 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, 3 citations in OpenAlex.
- HMGB3: A pivotal orchestrator of therapy resistance and cancer stemness in human malignancies (Review).Oncology reports · 2026Review
- Article
- Downregulation of ITIH3 contributes to cisplatin-based chemotherapy resistance in ovarian carcinoma via the Bcl-2 mediated anti-apoptosis signaling pathway.Oncology letters · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Glaucocalyxin A (GLA) is an ent-kaurene diterpenoid from Methods: The expression of HMGB3 in EOC tissues was analyzed by GEPIA and immunohistochemistry. Cell proliferation was determined using CCK-8 and colony formation assays. Cell invasion, migration, and apoptosis were detected using Transwell, wound healing, and flow cytometry assays, respectively. Interactions between HMGB3 and miRNAs were predicted using ENCORI and validated using a dual-luciferase assay. mRNA expression levels of HMGB3 and miRNAs were measured using qPCR. Protein expression levels of HMGB3, E-cadherin, N-cadherin, Wnt3a,β-catenin, Bcl-2, and Bax were measured by western blotting. A tumor xenograft model was established to validate the efficacy and mechanism of GLA Results: HMGB3 was upregulated in EOC tissues and cells. GLA dose-dependently inhibited EOC cell proliferation and epithelial-mesenchymal transition (EMT). HMGB3 overexpression promoted proliferation, invasion, migration, and EMT, and suppressed the apoptosis of EOC cells. In addition, miR-374b-5p was targeted by HMGB3, and its overexpression hindered malignant characteristics of EOC cells. HMGB3 overexpression weakened antitumor effects of GLA and miR-374b-5p in EOC cells. Moreover, the Wnt-β-catenin pathway was inhibited by the GLA-mediated miR-374b-5p/HMGB3 axis. Conclusions: GLA suppressed the malignant progression of EOC by regulating the miR-374b-5p/HMGB3/Wnt-β-catenin pathway axis.
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