Ovarian Tumor Microenvironment Signaling: Convergence on the Rac1 GTPase
AbstractThe tumor microenvironment for epithelial ovarian cancer is complex and rich in bioactive molecules that modulate cell-cell interactions and stimulate numerous signal transduction cascades. These signals ultimately modulate all aspects of tumor behavior including progression, metastasis and therapeutic response. Many of the signaling pathways converge on the small GTPase Ras-related C3 botulinum toxin substrate (Rac)1. In addition to regulating actin cytoskeleton remodeling necessary for tumor cell adhesion, migration and invasion, Rac1 through its downstream effectors, regulates cancer cell survival, tumor angiogenesis, phenotypic plasticity, quiescence, and resistance to therapeutics. In this review we discuss evidence for Rac1 activation within the ovarian tumor microenvironment, mechanisms of Rac1 dysregulation as they apply to ovarian cancer, and the potential benefits of targeting aberrant Rac1 activity in this disease. The potential for Rac1 contribution to extraperitoneal dissemination of ovarian cancer is addressed. View Full-Text
A printed edition of this Special Issue is available here.
Share & Cite This Article
Hudson, L.G.; Gillette, J.M.; Kang, H.; Rivera, M.R.; Wandinger-Ness, A. Ovarian Tumor Microenvironment Signaling: Convergence on the Rac1 GTPase. Cancers 2018, 10, 358.
Hudson LG, Gillette JM, Kang H, Rivera MR, Wandinger-Ness A. Ovarian Tumor Microenvironment Signaling: Convergence on the Rac1 GTPase. Cancers. 2018; 10(10):358.Chicago/Turabian Style
Hudson, Laurie G.; Gillette, Jennifer M.; Kang, Huining; Rivera, Melanie R.; Wandinger-Ness, Angela. 2018. "Ovarian Tumor Microenvironment Signaling: Convergence on the Rac1 GTPase." Cancers 10, no. 10: 358.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.