Suramin inhibits cullin-RING E3 ubiquitin ligases

April 5, 2016

Compound stock solutions in DMSO were titrated into 384-well plates using an HP D300 digital dispenser

Cullin-RING E3 ubiquitin ligases (CRL) control a myriad of biological processes by directing numerous protein substrates for proteasomal degradation. Key to CRL activity is the recruitment of the E2 ubiquitin-conjugating enzyme Cdc34 through electrostatic interactions between E3's cullin conserved basic canyon and the acidic C terminus of the E2 enzyme. This report demonstrates that a small-molecule compound, suramin, can inhibit CRL activity by disrupting its ability to recruit Cdc34. Suramin, an antitrypansomal drug that also possesses antitumor activity, was identified here through a fluorescence-based high-throughput screen as an inhibitor of ubiquitination. Suramin was shown to target cullin 1's conserved basic canyon and to block its binding to Cdc34. Suramin inhibits the activity of a variety of CRL complexes containing cullin 2, 3, and 4A. When introduced into cells, suramin induced accumulation of CRL substrates. These observations help develop a strategy of regulating ubiquitination by targeting an E2-E3 interface through small-molecule modulators.

Wu, K; Chong, RA; Yu, Q; Bai, J; Spratt, DE; Ching, K; Lee, C; Miao, H; Tappin, I; Hurwitz, J; Zheng, N; Shaw, GS; Sun, Y; Felsenfeld, DP; Sanchez, R; Zheng, JN; Pan, ZQ;

Journal: Proc. Natl. Acad. Sci. U.S.A. Pages: E2011-E2018

Original article (27001857)