STAT3 inhibition by WP1066 suppresses the growth and invasiveness of bladder cancer cells.
By: Yujiro Tsujita, Akio Horiguchi, Shinsuke Tasaki, Makoto Isono, Takako Asano, Keiichi Ito, Tomohiko Asano, Yoshine Mayumi, Toshihiro Kushibiki

Department of Urology, National Defense Medical College, Tokorozawa, Saitama 359-8513, Japan.
2017-04-01; doi: 10.3892/or.2017.5902
Abstract

Signal transducer and activator of transcription 3 (STAT3) regulates the expression of genes mediating cell survival, proliferation and angiogenesis and is aberrantly activated in various types of malignancies, including bladder cancer. We examined whether it could be a novel therapeutic target for bladder cancer using the STAT3 inhibitor WP1066. In T24 and UMUC-3 bladder cancer cells, 5 µM WP1066 prevented the phosphorylation of STAT3 and 2.5 µM WP1066 decreased cell survival and proliferation significantly (P<0.01). WP1066 also induced apoptosis accompanied by the suppression of the expression of Bcl-2 and Bcl-xL in T24 cells. Moreover, the covered area in a wound and the number of cells invading through a Matrigel chamber decreased significantly (P<0.01) when cells were treated with WP1066. The activities of MMP-2 and MMP-9 were also decreased by treatment with 10 µM WP1066. Our results revealed that using WP1066 to inhibit the STAT3 signaling pathway suppressed the viability and invasiveness of bladder cancer cells effectively and could be a novel therapeutic strategy against bladder cancer.





PMID:28849140






Copyright 2026 InterMDnet | Privacy Policy | Disclaimer | System Requirements