Department of Laboratory Science, Zengcheng District People's Hospital of Guangzhou (BoJi-Affiliated Hospital of Sun Yat-sen University), Guangzhou, 511300, China.
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Sci Rep. 2017 Mar 23;7(1):367. doi: 10.1038/s41598-017-00517-w.
Survivin is a proto-oncogene biomarker known for its anti-apoptotic and cell cycle regulating properties induced by the activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway. In the context of non-cancer pathology, such as rheumatoid arthritis (RA), survivin has emerged as a feature associated with severe joint damage and poor treatment response. Phosphatase and tensin homolog (PTEN) is a phosphatase antagonizing all classes of PI3K. The interplay between survivin oncogenic mechanisms and proliferation suppression networks in RA has remained largely elusive. This study investigated the effect of PTEN on survivin gene expression in rheumatiod arthritis fibroblast-like synoviocyte (RA-FLS). We showed for the first time that the suppression of RA-FLS was mediated by PTEN involving survivin silencing. Considering that survivin suppressants are currently available in clinical trials and clinical use, their effects in RA-FLS support a probably RA therapy to clinical practice.
Survivin 是一种原癌基因生物标志物，其抗细胞凋亡和细胞周期调节特性是通过磷酸肌醇 3-激酶 (PI3K)/Akt 途径的激活诱导的。在非癌症病理情况下，如类风湿关节炎 (RA)，Survivin 已成为与严重关节损伤和治疗反应不佳相关的特征。磷酸酶和张力蛋白同源物 (PTEN) 是一种磷酸酶，可拮抗所有类型的 PI3K。Survivin 致癌机制与 RA 中增殖抑制网络之间的相互作用在很大程度上仍未被揭示。本研究调查了 PTEN 对类风湿关节炎成纤维样滑膜细胞 (RA-FLS) 中 survivin 基因表达的影响。我们首次表明，PTEN 通过沉默 survivin 介导了对 RA-FLS 的抑制。考虑到目前正在临床试验和临床中使用 survivin 抑制剂，它们在 RA-FLS 中的作用支持将可能的 RA 治疗方法应用于临床实践。
