Wnt/beta-catenin-pathway as a molecular target for future anti-cancer therapeutics.
Conventional chemotherapeutic drugs used for the treatment of cancer patients in advanced stages have yielded only limited benefit, regarding survival time not to mention cure of the patients. To improve the clinical outcome of cancer, agents aimed at novel molecular targets are required. Colorectal and many other cancers are caused by hyperactivity of the Wnt/beta-catenin signaling pathway that results in constitutive beta-catenin mediated transactivation of T cell factor (Tcf)-dependent genes. Accordingly, disruption of this signaling pathway holds promise for the development of new anti-cancer drugs. Our study describes recent therapeutic strategies to interfere with tumor growth by blocking the unrestricted activation of the Wnt/beta-catenin pathway. The antagonists, which may become lead compounds of new anticancer therapeutics include established drugs in new application areas, recombinant biomolecules, virus mediated selective cell killing, and small molecules, disrupting protein-protein interactions.
Institute of Molecular Pathology, University of Heidelberg, Im Neuenheimer Feld 220/221, D-69120 Heidelberg, Germany. susanne.dihlmann@med.uni-heidelberg.de
Susanne
S
Dihlmann
Magnus
M
von Knebel Doeberitz
D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D003598:Cytoskeletal Proteins / Q000502:physiology*; D005544:Forecasting; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology*; D009369:Neoplasms / Q000188:drug therapy*; D015398:Signal Transduction; D015534:Trans-Activators / Q000502:physiology*; D051153:Wnt Proteins; D051176:beta Catenin
D000970:Antineoplastic Agents; C495270:CTNNB1 protein, human; D003598:Cytoskeletal Proteins; D036341:Intercellular Signaling Peptides and Proteins; D015534:Trans-Activators; D051153:Wnt Proteins; D051176:beta Catenin