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细胞朊蛋白通过其糖基化状态抵抗细胞凋亡依赖于口腔 HSC-2 和结肠 LS 174T 癌细胞。

Resistance against apoptosis by the cellular prion protein is dependent on its glycosylation status in oral HSC-2 and colon LS 174T cancer cells.

机构信息

Department of Biomedical Science, Faculty of Science, Universiti Tunku Abdul Rahman, Perak Campus, Kampar, Perak, Malaysia.

出版信息

Cancer Lett. 2011 Jul 1;306(1):111-9. doi: 10.1016/j.canlet.2011.02.040. Epub 2011 Mar 24.

Abstract

Most studies have focused on the role of the cellular prion protein (PrP(C)) in neurodegenerative diseases, whereas the function of this ubiquitous protein outside the nervous system remains elusive. Therefore, the anti-apoptotic property of PrP(C) in oral squamous cell carcinoma (HSC-2) and colon adenocarcinoma (LS 174T) was evaluated in this study, by stable shRNA knockdown and overexpression, respectively. PrP(C) confers resistance against oxidative stress-apoptosis as indicated by MTT assay, Annexin V-FITC/PI and DCFH-DA staining, but this property is abolished upon N-glycosylation inhibition by tunicamycin. Our results indicate that the inhibition of glycosylation in cancer cells overexpressing PrP(C) could represent a potential therapeutic target.

摘要

大多数研究都集中在细胞朊病毒蛋白 (PrP(C)) 在神经退行性疾病中的作用,而该蛋白在神经系统外的功能仍然难以捉摸。因此,本研究通过稳定的 shRNA 敲低和过表达,分别评估了 PrP(C) 在口腔鳞状细胞癌 (HSC-2) 和结肠腺癌 (LS 174T) 中的抗凋亡特性。MTT 检测、Annexin V-FITC/PI 和 DCFH-DA 染色表明,PrP(C) 赋予细胞抵抗氧化应激凋亡的能力,但这种特性在经 tunicamycin 抑制 N-糖基化后被消除。我们的结果表明,抑制过表达 PrP(C) 的癌细胞中的糖基化可能代表一个潜在的治疗靶点。

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