Journal
BIOLOGICAL CHEMISTRY
Volume 398, Issue 7, Pages 721-735Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/hsz-2016-0326
Keywords
adhesion; CAM-DR; CAM-RR; EGFR; integrin; resistome
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Funding
- Deutsche Krebshilfe [108976]
- Wilhelm Sander Stiftung [2012.149.1]
- BEMER Int. AG (Liechtenstein)
- European Union (RADIATE) [642623]
- EFRE Europaische Fonds fur regionale Entwicklung, Europa fordert Sachsen [100066308]
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Cell adhesion-mediated resistance limits the success of cancer therapies and is a great obstacle to overcome in the clinic. Since the 1990s, where it became clear that adhesion of tumor cells to the extracellular matrix is an important mediator of therapy resistance, a lot of work has been conducted to understand the fundamental underlying mechanisms and two paradigms were deduced: cell adhesion-mediated radioresistance (CAM-RR) and cell adhesion-mediated drug resistance (CAM-DR). Preclinical work has evidently demonstrated that targeting of integrins, adapter proteins and associated kinases comprising the cell adhesion resistome is a promising strategy to sensitize cancer cells to both radiotherapy and chemotherapy. Moreover, the cell adhesion resistome fundamentally contributes to adaptation mechanisms induced by radiochemotherapy as well as molecular drugs to secure a balanced homeostasis of cancer cells for survival and growth. Intriguingly, this phenomenon provides a basis for synthetic lethal targeted therapies simultaneously administered to standard radiochemotherapy. In this review, we summarize and highlight targeting strategies to override CAM-RR and CAM-DR.
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