RHO–GTPases and cancer
By Erik Sahai, C. Marshall. Nature Reviews. Cancer, 2002
1,555 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/37bd7dca1af806f144b80dd10aca4e00e7e14b1b
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Citations in the corpus
- A Pleiotropically Acting microRNA, miR-31, Inhibits Breast Cancer Metastasis (2009, neutral): “Guided by this gene ontology analysis, we cloned the 30 UTRs of 16 putative miR-31 targets from these overrepresented categories, including several implicated in tumor invasion (Sahai and Marshall, 2002; McClatchey, 2003), into a luciferase construct.”
- EMT, the cytoskeleton, and cancer cell invasion (2009, background): “In general, RhoGTPases affect almost all cell biological processes in a cell’s life [133–135].”
- MAP kinase signalling pathways in cancer (2007, background): “One important mechanism whereby ERK signalling may promote a more malignant phenotype is by disrupting Rho signalling pathways (Sahai and Marshall, 2002).”
- GTP‐binding proteins of the Rho/Rac family: regulation, effectors and functions in vivo (2007, background): “dysfunctional.(3,4) This crucial role has led to a comprehensive study on their mechanism of regulation, to the identification of additional elements of their signal transduction pathways, and to the characterization of their roles in vivo.”
- Human RAS Superfamily Proteins and Related GTPases (2004, background): “Mounting evidence supports the involvement of RHO proteins in cancer (189).”
- Rac and Rho GTPases in cancer cell motility control (2010, background): “Beside environmental regulation, MAT can also be induced by epigenetic expression of regulating factors.”
- Anoikis molecular pathways and its role in cancer progression. (2013, background): “In addition, this leads to the PI3K-dependent activation of Rac-1 and Cdc42 at the leading edge of the cell, which coordinate actin polymerization [187].”
- Mutant p53 as a guardian of the cancer cell (2018, neutral): “RhoA is frequently overexpressed or hyper-activated in tumors [21].”