The marine natural product trichobotrysin B inhibits proliferation and promotes apoptosis of human glioma cells via the IL-6-mediated STAT3/JAK signaling pathway

Glioma is the most common malignant tumor of the central nervous system. Drug-assisted chemotherapy is an important adjuvant treatment post-surgery, but currently, effective chemotherapy drugs for glioma are lacking. Expediting new and effective chemotherapy drugs is a persistent problem that needs to be solved. In this study, a tetramic acid derivative, trichobotrysin B, was extracted from the ascidian-derived fungus Trichobotrys effusa 4729 (denoted ADFTe4729). There is significant cytotoxicity of trichobotrysin B against glioma proliferation, which triggers apoptosis and cell cycle arrest. Furthermore, studies have found that trichobotrysin B inhibits glioma proliferation in a manner closely related to IL-6-mediated STAT3 phosphorylation and JAK2 activation. In conclusion, this study demonstrates that the small-molecule compound trichobotrysin B inhibits glioma proliferation and induces apoptosis through the IL-6-mediated STAT3/JAK2 signaling pathway, suggesting that trichobotrysin B has potential antiglioma efficiency and provides a new way to explore new small-molecule drugs with anticancer effects. [Display omitted] •Trichobotrysin B was extracted from the ascidian-derived fungus Trichobotrys effusa 4729.•Trichobotrysin B showed significant cytotoxicity against glioma proliferation.•Trichobotrysin B inhibits glioma proliferation via IL-6-mediated STAT3 phosphorylation and JAK2 activation.