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Hyperforin induces apoptosis through extrinsic/intrinsic pathways and inhibits EGFR / ERK / NF‐κB ‐mediated anti‐apoptotic potential in glioblastoma
Author(s) -
Hsu FeiTing,
Chen WeiTing,
Wu ChingTe,
Chung JingGung
Publication year - 2020
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22942
Subject(s) - hyperforin , mapk/erk pathway , signal transduction , apoptosis , chemistry , cancer research , epidermal growth factor receptor , kinase , pharmacology , hypericum perforatum , microbiology and biotechnology , biology , receptor , biochemistry
Glioblastoma is the most common primary brain tumor with poor survival rate and without effective treatment strategy. Notably, amplification and active mutation of epidermal growth factor receptor (EGFR) occur frequently in glioblastoma patient that may be a potential treatment target. Several studies indicated that various type of herbal compounds not only regulate anti‐depressant effect but also shown capacity to suppress glioblastoma growth via inducing apoptosis and inhibiting oncogene signaling transduction. Hyperforin, an herb compound derived from St. John's wort was used to treat depressive disorder by inhibiting neuronal reuptake of several neurotransmitters. Although hyperforin can reduce matrix metallopeptidases‐2 (MMPs) and ‐9‐mediated metastasis of glioblastoma, the detail mechanism of hyperforin on glioblastoma is remaining unclear. Here, we suggested that hyperforin may induce extrinsic/intrinsic apoptosis and suppress anti‐apoptotic related proteins expression of glioblastoma. We also indicated that hyperforin‐mediated anti‐apoptotic potential of glioblastoma was correlated to inactivation of EGFR/extracellular signal‐regulated kinases (ERK)/nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling.