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Cutting the Brakes on Ras - Cytoplasmic GAPs as Targets of Inactivation in Cancer

Bellazzo, Arianna
•
Collavin, Licio
2020
  • journal article

Periodico
CANCERS
Abstract
The Ras pathway is frequently deregulated in cancer, actively contributing to tumor development and progression. Oncogenic activation of the Ras pathway is commonly due to point mutation of one of the three Ras genes, which occurs in almost one third of human cancers. In the absence of Ras mutation, the pathway is frequently activated by alternative means, including the loss of function of Ras inhibitors. Among Ras inhibitors, the GTPase-Activating Proteins (RasGAPs) are major players, given their ability to modulate multiple cancer-related pathways. In fact, most RasGAPs also have a multi-domain structure that allows them to act as scaffold or adaptor proteins, affecting additional oncogenic cascades. In cancer cells, various mechanisms can cause the loss of function of Ras inhibitors; here, we review the available evidence of RasGAP inactivation in cancer, with a specific focus on the mechanisms. We also consider extracellular inputs that can affect RasGAP levels and functions, implicating that specific conditions in the tumor microenvironment can foster or counteract Ras signaling through negative or positive modulation of RasGAPs. A better understanding of these conditions might have relevant clinical repercussions, since treatments to restore or enhance the function of RasGAPs in cancer would help circumvent the intrinsic difficulty of directly targeting the Ras protein.
DOI
10.3390/cancers12103066
WOS
WOS:000584119500001
Archivio
http://hdl.handle.net/11368/2973570
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85093649130
https://www.mdpi.com/2072-6694/12/10/3066
Diritti
open access
FVG url
https://arts.units.it/bitstream/11368/2973570/1/Bellazzo Cancers_2020.pdf
Soggetti
  • GTPase-Activating Pro...

  • RAS oncogene

  • cell signaling

  • mechanisms of transfo...

  • signal transduction

  • tumor suppressor gene...

Web of Science© citazioni
6
Data di acquisizione
Mar 23, 2024
Visualizzazioni
1
Data di acquisizione
Apr 19, 2024
Vedi dettagli
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