Back to Journals » Drug Design, Development and Therapy » Volume 9

Repurposing paclitaxel for the treatment of fibrosis: indication discovery for existing drugs

Authors Chen X, Duan W, Zhou S

Received 31 July 2015

Accepted for publication 31 July 2015

Published 7 September 2015 Volume 2015:9 Pages 4869—4871

DOI https://doi.org/10.2147/DDDT.S87771

Checked for plagiarism Yes


Xiao-Wu Chen,1 Wei Duan,2 Shu-Feng Zhou3

1Department of General Surgery, The First People’s Hospital of Shunde, Southern Medical University, Shunde, Foshan, Guangdong, People’s Republic of China; 2School of Medicine, Deakin University, Waurn Ponds, Victoria, Australia; 3Department of Pharmaceutical Science, College of Pharmacy, University of South Florida, Tampa, FL, USA

In the recently published paper by Zhang et al1 in Drug Des Develop Ther, the authors have evaluated the role of signal transducer and activator of transcription 3 (STAT3) in the antifibrotic activity of paclitaxel in vitro and in mice. They have reported that the treatment of paclitaxel at 2–4 μM reduced the level of phosphorylated STAT3 at Tyr705 in a dose- and time-dependent manner, and downregulated the expression of fibronectin, α-smooth muscle actin (α-SMA), and collagen I in cultured rat renal interstitial fibroblast NRK-49F cells derived from normal kidney. Treatment of the cells with the selective STAT3 inhibitor S3I-201 at 50 mM suppressed the expression of fibronectin, α-SMA, and collagen I in NRK-49F cells. However, S3I-201 treatment increased the expression of phosphorylated STAT1 but did not affect that of phosphorylated STAT5M. The immunoprecipitation assay has revealed that paclitaxel inhibited the STAT3 activity by disrupting the binding of STAT3 with tubulin independently of the effect on STAT3 phosphorylation and by inhibiting STAT3 nucleus translocation.1

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]