ArticleJournal of hematology & oncology2019
Ilamycin C induces apoptosis and inhibits migration and invasion in triple-negative breast cancer by suppressing IL-6/STAT3 pathway.
Article in Journal of hematology & oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Role of STAT3 signaling pathway in breast cancer.Cell communication and signaling : CCS · 2020Pooled it
- Escherichia coli DH5α-loaded fenugreek extract: an effective anticancer combination against human breast cancer cell lines.Applied microbiology and biotechnology · 2026Article
- Oncogenic cell fate decision in breast epithelial cells I: growth factors and mechanisms.Research square · 2026Article
- Arctigenin ameliorates neointima formation induced by vascular injury by inhibiting inflammatory response and proliferation through the IL-6/JAK2/STAT3 pathway.Molecular and cellular biochemistry · 2026Article
- Targeting STAT3 in Breast Cancer Using Innovative Natural and Synthetic Scaffolds to Trigger Apoptosis, Autophagy, and Halt Tumor Progression.Current drug targets · 2026Review
- YAP-induced MAML1 cooperates with STAT3 to drive hepatocellular carcinoma progression.Experimental hematology & oncology · 2025Article
- Article
- Discovery of Natural Compound α-Hederin via Large-Scale Screening as a Targeted JAK/STAT3 Inhibitor for Ovarian Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting the Tumor Immune Microenvironment in Triple-Negative Breast Cancer: The Promise of Polyphenols.Cancers · 2025Review
- Integrative systems biology and in-vitro analysis of cryptolepine's therapeutic role in breast cancer.Discover oncology · 2025Article
- Enhancing rufomycin production by CRISPR/Cas9-based genome editing and promoter engineering inSynthetic and systems biotechnology · 2025Article
- Characterization of RufT Thioesterase Domain Reveals Insights into Rufomycin Cyclization and the Biosynthetic Origin of Rufomyazine.ACS chemical biology · 2025Article
- Fabrication of zinc oxide nanoparticles usingOpen life sciences · 2025Article
- Prospects of marine-derived compounds as potential therapeutic agents for glioma.Pharmaceutical biology · 2024Review
- Unraveling Stereochemical Structure-Activity Relationships of Sesquiterpene Lactones for Inhibitory Effects on STAT3 Activation.Biomolecules & therapeutics · 2024Article
- Rapid Peptide Cyclization Inspired by the Modular Logic of Nonribosomal Peptide Synthetases.Journal of the American Chemical Society · 2024Article
- Influence of heterochirality on the structure, dynamics, biological properties of cyclic(PFPF) tetrapeptides obtained by solvent-free ball mill mechanosynthesis.Scientific reports · 2024Article
- Small protein blockers of human IL-6 receptor alpha inhibit proliferation and migration of cancer cells.Cell communication and signaling : CCS · 2024Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor prognosis, and its treatment remains a challenge due to few targeted medicines and high risk of relapse, metastasis, and drug resistance. Thus, more effective drugs and new regimens for the therapy of TNBC are urgently needed. Ilamycins are a kind of cyclic peptides and produced by Streptomyces atratus and Streptomyces islandicus with effective anti-tuberculosis activity. Ilamycin C is a novel compound isolated from the deep South China Sea-derived Streptomyces atratus SCSIO ZH16 and exhibited a strong cytotoxic activity against several cancers including breast cancer cell line MCF7. However, the cytotoxic activity of Ilamycin C to TNBC cells and a detailed antitumor mechanism have not been reported.
methodsCCK-8 assays were used to examine cell viability and cytotoxic activity of Ilamycin C to TNBC, non-TNBC MCF7, and nonmalignant MCF10A cells. EdU assays and flow cytometry were performed to assess cell proliferation and cell apoptosis. Transwell migration and Matrigel invasion assays were utilized to assess the migratory and invading capacity of TNBC cells following the treatment of Ilamycin C. The expressions of proteins were detected by western blot.
resultsIn this study, we found that Ilamycin C has more preferential cytotoxicity in TNBC cells than non-TNBC MCF7 and nonmalignant MCF10A cells. Notably, our studies revealed the mechanism that Ilamycin C can induce Bax/Bcl-2-related caspase-dependent apoptosis and inhibit migration and invasion through MMP2/MMP9/vimentin/fascin in TNBC by suppressing IL-6-induced STAT3 phosphorylation.
conclusionsThis study provides the first evidence that Ilamycin C has significant implications for the potential as a novel IL-6/STAT3 inhibitor for TNBC treatment in the future.
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