Rac1 Signaling: From Intestinal Homeostasis to Colorectal Cancer Metastasis.
E-cadherin
Rac1
Wnt signaling
alternative splicing
colorectal cancer
epithelial mesenchymal transition
intestine
invasiveness
metastasis
small GTPase
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
12 Mar 2020
12 Mar 2020
Historique:
received:
17
02
2020
revised:
06
03
2020
accepted:
08
03
2020
entrez:
18
3
2020
pubmed:
18
3
2020
medline:
18
3
2020
Statut:
epublish
Résumé
The small GTPase Rac1 has been implicated in a variety of dynamic cell biological processes, including cell proliferation, cell survival, cell-cell contacts, epithelial mesenchymal transition (EMT), cell motility, and invasiveness. These processes are orchestrated through the fine tuning of Rac1 activity by upstream cell surface receptors and effectors that regulate the cycling Rac1-GDP (off state)/Rac1-GTP (on state), but also through the tuning of Rac1 accumulation, activity, and subcellular localization by post translational modifications or recruitment into molecular scaffolds. Another level of regulation involves Rac1 transcripts stability and splicing. Downstream, Rac1 initiates a series of signaling networks, including regulatory complex of actin cytoskeleton remodeling, activation of protein kinases (PAKs, MAPKs) and transcription factors (NFkB, Wnt/β-catenin/TCF, STAT3, Snail), production of reactive oxygen species (NADPH oxidase holoenzymes, mitochondrial ROS). Thus, this GTPase, its regulators, and effector systems might be involved at different steps of the neoplastic progression from dysplasia to the metastatic cascade. After briefly placing Rac1 and its effector systems in the more general context of intestinal homeostasis and in wound healing after intestinal injury, the present review mainly focuses on the several levels of Rac1 signaling pathway dysregulation in colorectal carcinogenesis, their biological significance, and their clinical impact.
Identifiants
pubmed: 32178475
pii: cancers12030665
doi: 10.3390/cancers12030665
pmc: PMC7140047
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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