Enhanced YAP/TAZ activity is emerging as common trait of multiple solid tumors in humans. Strikingly, in mouse models, adult organs lacking YAP/TAZ are unable to develop tumors without overt side effects for normal tissue homeostasis, making YAP/TAZ prime candidates for cancer therapy. That said, YAP/TAZ have physiological functions during tissue repair, being essential for organ regeneration after injury. YAP/TAZ are typically inactive in normal tissues but potently induced by mechanical and physical cues that the cell receives from its microenvironment, such as extracellular matrix stiffness and topology, and 3D architectural features of the tissue. I will focus on new discoveries on the mechanisms by which YAP/TAZ are controlled by mechanotransduction, and on YAP/TAZ as reprogramming factors in epithelial cells. Indeed, in normal tissues YAP/TAZ activation turns more differentiated normal cells into cells endowed with stem-like properties; in tumors, YAP/TAZ convert non-stem tumor cells into cancer-stem cells, increasing tumor aggressiveness and fueling metastasis. I will also expand on these mechanisms, providing new hints for therapeutic intervention.

Citation Format: Stefano Piccolo. YAP/TAZ activity as hallmark of cancer: Biologic properties, upstream regulations, and downstream targets [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr SY40-02.

©2019 American Association for Cancer Research.
2019
American Association for Cancer Research.