RASSF1A Tumour Suppressor: Target the Network for Effective Cancer Therapy

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Title: RASSF1A Tumour Suppressor: Target the Network for Effective Cancer Therapy
Authors: García-Gutiérrez, LucíaMcKenna, StephanieKolch, WalterMatallanas, David
Permanent link: http://hdl.handle.net/10197/11883
Date: 17-Jan-2020
Online since: 2021-01-25T13:17:46Z
Abstract: The RASSF1A tumour suppressor is a scaffold protein that is involved in cell signalling. Increasing evidence shows that this protein sits at the crossroad of a complex signalling network, which includes key regulators of cellular homeostasis, such as Ras, MST2/Hippo, p53, and death receptor pathways. The loss of expression of RASSF1A is one of the most common events in solid tumours and is usually caused by gene silencing through DNA methylation. Thus, re-expression of RASSF1A or therapeutic targeting of effector modules of its complex signalling network, is a promising avenue for treating several tumour types. Here, we review the main modules of the RASSF1A signalling network and the evidence for the effects of network deregulation in different cancer types. In particular, we summarise the epigenetic mechanism that mediates RASSF1A promoter methylation and the Hippo and RAF1 signalling modules. Finally, we discuss different strategies that are described for re-establishing RASSF1A function and how a multitargeting pathway approach selecting druggable nodes in this network could lead to new cancer treatments.
Funding Details: Science Foundation Ireland
Type of material: Journal Article
Publisher: MDPI
Journal: Cancers
Volume: 12
Issue: 1
Copyright (published version): 2020 the Authors
Keywords: GeneticsCancerRASSF1ATumour suppressorTherapyApoptosisHippo pathwayDNMTP
DOI: 10.3390/cancers12010229
Language: en
Status of Item: Peer reviewed
ISSN: 2072-6694
This item is made available under a Creative Commons License: https://creativecommons.org/licenses/by/3.0/ie/
Appears in Collections:Conway Institute Research Collection
SBI Research Collection
Medicine Research Collection

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