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Updated: Mar 5, 2026

Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
Published on: October 16, 2016
Rheumatoid Arthritis Fibroblast-like Synoviocyte Suppression Mediated by PTEN Involves Survivin Gene Silencing
Danna Chen1,2, Dongdong Liu2, Dan Liu2
1Department of Laboratory Science, Zengcheng District People's Hospital of Guangzhou (BoJi-Affiliated Hospital of Sun Yat-sen University), Guangzhou, 511300, China.
Abstract:
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.
Insights
This study reveals that PTEN suppresses survivin, a key protein in rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLS). This finding suggests PTEN-based therapies could be a novel treatment for RA joint damage.
Area of Science:
- Molecular Biology
- Immunology
- Rheumatology
Background:
- Survivin, a proto-oncogene, promotes cell survival and proliferation via the PI3K/Akt pathway.
- In rheumatoid arthritis (RA), elevated survivin correlates with severe joint damage and poor treatment outcomes.
- The role of PTEN, a PI3K antagonist, in regulating survivin in RA remains unclear.
Purpose of the Study:
- To investigate the effect of PTEN on survivin gene expression in RA fibroblast-like synoviocytes (RA-FLS).
- To elucidate the interplay between PTEN and survivin in the context of RA pathogenesis.
Main Methods:
- Primary RA-FLS were utilized to examine PTEN's influence on survivin expression.
- Gene expression analysis was performed to quantify survivin levels following PTEN modulation.
Main Results:
- PTEN was found to suppress survivin gene expression in RA-FLS.
- This suppression by PTEN was identified as the mechanism mediating the inhibition of RA-FLS proliferation.
- The study demonstrated PTEN-mediated survivin silencing in RA-FLS for the first time.
Conclusions:
- PTEN plays a critical role in regulating survivin expression in RA pathogenesis.
- Targeting PTEN could represent a novel therapeutic strategy for managing rheumatoid arthritis.
- Survivin suppressants, potentially acting through PTEN, may offer new treatment avenues for RA patients.
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