Quambalarine B, a Secondary Metabolite from Quambalaria cyanescens with Potential Anticancer Properties
Language English Country United States Media print-electronic
Document type Journal Article
- MeSH
- Antineoplastic Agents blood chemistry isolation & purification pharmacology MeSH
- Basidiomycota chemistry MeSH
- Phosphorylation MeSH
- Jurkat Cells drug effects MeSH
- Ribosomal Protein S6 Kinases, 70-kDa MeSH
- Drug Screening Assays, Antitumor MeSH
- Leukocytes, Mononuclear drug effects MeSH
- Humans MeSH
- Molecular Structure MeSH
- Naphthoquinones blood chemical synthesis chemistry isolation & purification pharmacology MeSH
- Cell Proliferation drug effects MeSH
- Signal Transduction physiology MeSH
- TOR Serine-Threonine Kinases MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- 3-hexanoyl-2,5,7,8-tetrahydroxy-1,4-naphthoquinone MeSH Browser
- Antineoplastic Agents MeSH
- Ribosomal Protein S6 Kinases, 70-kDa MeSH
- MTOR protein, human MeSH Browser
- Naphthoquinones MeSH
- TOR Serine-Threonine Kinases MeSH
Quambalarine B (QB) is a secondary metabolite produced by the basidiomycete Quambalaria cyanescens with potential anticancer activity. Here we report that QB at low micromolar concentration inhibits proliferation of several model leukemic cell lines (Jurkat, NALM6, and REH), whereas higher concentrations induce cell death. By contrast, the effect of QB on primary leukocytes (peripheral blood mononuclear cells) is significantly milder with lower toxicity and cytostatic activity. Moreover, QB inhibited expression of the C-MYC oncoprotein and mRNA expression of its target genes, LDHA, PKM2, and GLS. Finally, QB blocked the phosphorylation of P70S6K, a downstream effector kinase in mTOR signaling that regulates translation of C-MYC. This observation could explain the molecular mechanism behind the antiproliferative and cytotoxic effects of QB on leukemic cells. Altogether, our results establish QB as a promising molecule in anticancer treatment.
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