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鞣花酸通过抑制(免疫)蛋白酶体的活性诱导人胶质母细胞瘤 U251 细胞凋亡。

Corilagin induces human glioblastoma U251 cell apoptosis by impeding activity of (immuno)proteasome.

机构信息

Medical Research Center, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong 272029, P.R. China.

Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, VA 22908, USA.

出版信息

Oncol Rep. 2021 Apr;45(4). doi: 10.3892/or.2021.7985. Epub 2021 Mar 2.

DOI:10.3892/or.2021.7985
PMID:33649855
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7905533/
Abstract

Glioma is a type of common primary intracranial tumor, which is difficult to treat. It has been confirmed by research that corilagin (the primary active constituent of the matsumura leafflower herb) has significant antitumor effect. In particular, our previous research demonstrated that corilagin effectively promotes apoptosis of glioma U251 cells and has a synergistic effect when used with temozolomide. However, the mechanism by which corilagin causes apoptosis in U251 cells has yet to be investigated. Proteasomes are catalytic centers of the ubiquitin‑proteasome system, which is the major protein degradation pathway in eukaryotic cells; they are primarily responsible for the degradation of signal molecules, tumor suppressors, cyclins and apoptosis inhibitors and serve an important role in tumor cell proliferation and apoptosis. The present study investigated the pro‑apoptotic effect of corilagin on glioma U251 cells and confirmed that decreased proteasome activity and expression levels serve an important role in corilagin‑induced U251 cell apoptosis.

摘要

脑胶质瘤是一种常见的原发性颅内肿瘤,难以治疗。研究已证实,鞣花酸(山茶花属植物的主要活性成分)具有显著的抗肿瘤作用。特别是,我们之前的研究表明,鞣花酸可有效促进脑胶质瘤 U251 细胞凋亡,并与替莫唑胺具有协同作用。然而,鞣花酸导致 U251 细胞凋亡的机制尚未得到研究。蛋白酶体是泛素蛋白酶体系统的催化中心,是真核细胞中主要的蛋白质降解途径;它们主要负责降解信号分子、肿瘤抑制因子、细胞周期蛋白和凋亡抑制剂,在肿瘤细胞增殖和凋亡中发挥重要作用。本研究探讨了鞣花酸对脑胶质瘤 U251 细胞的促凋亡作用,并证实蛋白酶体活性和表达水平的降低在鞣花酸诱导的 U251 细胞凋亡中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/b686a77166b2/or-45-04-7985-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/77d1aa06736e/or-45-04-7985-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/8e2cdcbc713d/or-45-04-7985-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/c2ae9e7ed2b0/or-45-04-7985-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/499145505735/or-45-04-7985-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/d4847855e890/or-45-04-7985-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/f7360031a46b/or-45-04-7985-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/b686a77166b2/or-45-04-7985-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/77d1aa06736e/or-45-04-7985-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/8e2cdcbc713d/or-45-04-7985-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/c2ae9e7ed2b0/or-45-04-7985-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/499145505735/or-45-04-7985-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/d4847855e890/or-45-04-7985-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/f7360031a46b/or-45-04-7985-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/7905533/b686a77166b2/or-45-04-7985-g06.jpg

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