Cancers | |
Rho Family GTPases in Cancer | |
Suranganie Dharmawardhane1  | |
[1] Department of Biochemistry, School of Medicine, University of Puerto Rico Medical Sciences Campus, San Juan, PR 00936, USA; | |
关键词: Rho GTPases; cancer; targeted therapy; Rho; Rac; Cdc42; | |
DOI : 10.3390/cancers13061271 | |
来源: DOAJ |
【 摘 要 】
Rho GTPases have emerged as pivotal drivers of cancer metastasis in multiple cancer types. Therefore, understanding their dysregulation in cancer and developing drugs to inhibit their activation have become priorities. Even though oncogenic point mutations and splice variants have been reported in a number of cancers, Rho GTPases do not have to be mutated in cancer to drive cancer progression. Rho GTPases are activated via the dysregulation of the expression and/or activity of a myriad of oncogenic cell surface receptors, which converge on Rho GTPases by conveying signals through guanine nucleotide exchange factors (GEFs). In turn, Rho GTPases signal to multiple downstream effectors that regulate migration/invasion via de novo actin polymerization, cell polarization, metastasis, epithelial-to-mesenchymal transition (EMT), transcription, cell proliferation, cell cycle progression, apoptosis/survival, vesicle trafficking, angiogenesis, immune function, cell–cell and cell–substrate adhesions, and therapy resistance.
【 授权许可】
Unknown