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      Pectenotoxin-2 induces G1 arrest of the cell cycle in synovial fibroblasts of patients with rheumatoid arthritis.

      International Journal of Molecular Medicine

      Antirheumatic Agents, pharmacology, Arthritis, Rheumatoid, genetics, metabolism, Cell Cycle, drug effects, Cell Division, Cell Proliferation, Cyclin-Dependent Kinase 2, Cyclin-Dependent Kinase 6, Cyclin-Dependent Kinase Inhibitor p21, Fibroblasts, Furans, G1 Phase, Humans, Phosphorylation, Pyrans, Synovial Fluid

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          Abstract

          Rheumatoid arthritis (RA), a chronic inflammatory disease, is characterized by hyperplasia of the synovial fibroblasts, due in part to increased cell growth. This study investigated the mechanisms underlying the anti-proliferative action of pectenotoxin-2 (PTX-2), isolated from marine sponges, in synovial fibroblasts obtained from RA patients. PTX-2 concentration-dependently inhibited the growth of synovial fibroblasts, arresting them in the G1 phase of their cell cycle. The G1 arrest was correlated with down-regulation of cyclin D1 and cyclin-dependent kinase (Cdk) 6, with a concomitant up-regulation of the tumor suppressor, p53, and the Cdk inhibitor, p21 (WAF1/CIP1). Following PTX-2 treatment of synovial fibroblasts, an increased binding of p21 with Cdk2 and Cdk6 was paralleled by a significant decrease in retinoblastoma protein (pRB) phosphorylation and in the protein levels of E2F transcription factors. Thus, PTX-2 might help identify new therapeutic agents against RA-mediated hyperplasia of synovial fibroblasts.

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          Journal
          21373746
          10.3892/ijmm.2011.636

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