Rheumatoid Arthritis Fibroblast-like Synoviocyte Suppression Mediated by PTEN Involves Survivin Gene Silencing.
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.
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.
Danna
D
Chen
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Dongdong
D
Liu
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Dan
D
Liu
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Min
M
He
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Anping
A
Peng
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Jiarui
J
Xu
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Li
L
Lin
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Fudong
F
Luo
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Lin
L
Chen
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Xianzhang
X
Huang
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Junhua
J
Zhuang
Department of Laboratory Science, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China. jhxu1976@126.com.
Jianhua
J
Xu
D001172:Arthritis, Rheumatoid / Q000201:enzymology* / Q000235:genetics*; D002465:Cell Movement; D005260:Female; D005347:Fibroblasts / Q000201:enzymology; D020868:Gene Silencing; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D051034:Inhibitor of Apoptosis Proteins / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D051059:PTEN Phosphohydrolase / Q000378:metabolism*; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism; D000090063:Proto-Oncogene Mas; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D000077022:Survivin; D000070918:Synoviocytes / Q000201:enzymology*
C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D000077022:Survivin; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human