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Hyperforin induces apoptosis through extrinsic/intrinsic pathways and inhibits EGFR/ERK/NF-κB-mediated anti-apoptotic potential in glioblastoma
Environmental Toxicology ( IF 4.5 ) Pub Date : 2020-06-02 , DOI: 10.1002/tox.22942
Fei‐Ting Hsu, Wei‐Ting Chen, Ching‐Te Wu, Jing‐Gung Chung

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.

中文翻译:

Hyperforin 通过外在/内在途径诱导细胞凋亡并抑制胶质母细胞瘤中 EGFR/ERK/NF-κB 介导的抗凋亡潜力

胶质母细胞瘤是最常见的原发性脑肿瘤,存活率低且无有效治疗策略。值得注意的是,表皮生长因子受体(EGFR)的扩增和活性突变经常发生在胶质母细胞瘤患者中,这可能是一个潜在的治疗目标。几项研究表明,各种类型的草药化合物不仅可以调节抗抑郁作用,还可以通过诱导细胞凋亡和抑制癌基因信号转导来抑制胶质母细胞瘤的生长。Hyperforin 是一种源自圣约翰草的草药化合物,通过抑制几种神经递质的神经元再摄取来治疗抑郁症。虽然 hyperforin 可以减少基质金属肽酶-2 (MMPs) 和-9 介导的胶质母细胞瘤的转移,hyperforin 对胶质母细胞瘤的详细机制尚不清楚。在这里,我们建议金丝桃素可能诱导外在/内在细胞凋亡并抑制胶质母细胞瘤的抗凋亡相关蛋白的表达。我们还表明,hyperforin 介导的胶质母细胞瘤的抗凋亡潜力与 EGFR/细胞外信号调节激酶(ERK)/活化 B 细胞(NF-κB)信号传导的核因子κ-轻链增强子的失活有关。
更新日期:2020-06-02
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