丁硫氨酸通过触发内质网应激促进多形性胶质母细胞瘤细胞凋亡并与替莫唑胺协同作用。

IF 2.1
Anatomical record (Hoboken, N.J. : 2007) Pub Date : 2019-11-01 Epub Date: 2019-08-14 DOI:10.1002/ar.24194
Yafeng Sun, Xianhong Zhang
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引用次数: 8

摘要

多形性胶质母细胞瘤(GBM)是最常见的恶性胶质瘤。bufothiionine是Cinobufacini的主要活性成分之一。虽然丁硫氨酸的抗肿瘤作用已有报道,但其作用机制尚不清楚。本研究表明,丁硫氨酸对GBM细胞株U87和U373具有抗生长活性。进一步研究表明,丁硫氨酸触发内质网应激,促进U87和U373细胞凋亡。此外,我们的研究结果表明,丁硫氨酸与替莫唑胺(TMZ)具有协同抑制U87和U373细胞生长的作用。本研究结果为进一步研究丁硫氨酸治疗GBM的潜力提供了基础。生物工程学报,32(2):507 - 507,2019。©2019美国解剖学协会。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bufothionine Promotes Apoptosis via Triggering ER Stress and Synergizes with Temozolomide in Glioblastoma Multiforme Cells.

Glioblastoma multiforme (GBM) is the most common type of malignant glioma. Bufothionine is one of the major active ingredients of Cinobufacini. Although the antitumor activities of bufothionine have been reported, the underlying mechanism remains unclear. The present study showed that bufothionine exhibited antigrowth activities in GBM cell lines U87 and U373. Further investigation showed that bufothionine triggered endoplasmic reticulum (ER) stress to promote apoptosis in U87 and U373 cells. Moreover, our results showed that bufothionine exhibited synergistic activities with Temozolomide (TMZ) to suppress the growth of U87 and U373 cells. The findings in the present study provide basis for further investigation of the therapeutic potential of bufothionine in GBM. Anat Rec, 302:1950-1957, 2019. © 2019 American Association for Anatomy.

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