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Diallyl trisulfide inhibits proliferation, invasion and angiogenesis of glioma cells by inactivating Wnt/beta-catenin signaling

机译:二烯丙基三硫化物通过灭活wnt /β-catenin信号传导来抑制胶质瘤细胞的增殖,侵袭和血管生成

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摘要

Aberrant activation of Wnt/beta-catenin signaling leads to increased cell proliferation and survival and promotes the development of various human tumors, including glioma, one of the most common primary brain tumors. The treatment efficacy of many anticancer drugs remains limited or unsatisfactory and it is urgently necessary to develop effective and low-toxicity anticancer drugs or strategies, especially for glioma. Here, we report that diallyl trisulfide suppresses survival, migration, invasion and angiogenesis in glioma cells. These effects were associated with inhibition of the Wnt/beta-catenin signaling cascade, which was accompanied by decreased expression of LRP6, TRIM29 and Pygo2. A dual-luciferase reporter assay confirmed that DATS treatment decreased TCF/LEF-mediated transcription. Finally, a nude mouse tumorigenicity model was used to examine the biological effect of diallyl trisulfide in vivo. Consistent with the previous results, diallyl trisulfide inhibited proliferation, invasion and angiogenesis in glioma cells by suppressing Wnt/beta-catenin signaling.
机译:异常激活WNT /β-连环素信号传导导致细胞增殖和存活率增加,促进各种人类肿瘤的发展,包括胶质瘤,最常见的主要脑肿瘤之一。许多抗癌药物的治疗效果仍然有限或不令人满意,迫切需要开发有效和低毒性的抗癌药物或策略,特别是对于胶质瘤。在此,我们报告了二烯丙基三硫化物抑制胶质瘤细胞中的存活率,迁移,侵袭和血管生成。这些效应与WNT /β-连环蛋白信号传导级联的抑制相关,其伴随着LRP6,Trim29和Pygo2的表达降低。双荧光素酶报告总检测结果证实,DATS治疗降低了TCF / LEF介导的转录。最后,使用裸鼠瘤状模型来检查二烯丙基三硫化物在体内的生物学作用。通过抑制WNT /β-catenin信号传导,与先前的结果一致,三烯丙基三硫化物抑制胶质瘤细胞中的增殖,侵袭和血管生成。

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