Oncogenic Hijacking of the PIN1 Signaling Network.
cancer target therapy
organismal development
post-translational modification
prolyl-isomerase PIN1
signal transduction
tissue integrity
tumor development and progression
Journal
Frontiers in oncology
ISSN: 2234-943X
Titre abrégé: Front Oncol
Pays: Switzerland
ID NLM: 101568867
Informations de publication
Date de publication:
2019
2019
Historique:
received:
07
12
2018
accepted:
01
02
2019
entrez:
16
3
2019
pubmed:
16
3
2019
medline:
16
3
2019
Statut:
epublish
Résumé
Cellular choices are determined by developmental and environmental stimuli through integrated signal transduction pathways. These critically depend on attainment of proper activation levels that in turn rely on post-translational modifications (PTMs) of single pathway members. Among these PTMs, post-phosphorylation prolyl-isomerization mediated by PIN1 represents a unique mechanism of spatial, temporal and quantitative control of signal transduction. Indeed PIN1 was shown to be crucial for determining activation levels of several pathways and biological outcomes downstream to a plethora of stimuli. Of note, studies performed in different model organisms and humans have shown that hormonal, nutrient, and oncogenic stimuli simultaneously affect both PIN1 activity and the pathways that depend on PIN1-mediated prolyl-isomerization, suggesting the existence of evolutionarily conserved molecular circuitries centered on this isomerase. This review focuses on molecular mechanisms and cellular processes like proliferation, metabolism, and stem cell fate, that are regulated by PIN1 in physiological conditions, discussing how these are subverted in and hijacked by cancer cells. Current status and open questions regarding the use of PIN1 as biomarker and target for cancer therapy as well as clinical development of PIN1 inhibitors are also addressed.
Identifiants
pubmed: 30873382
doi: 10.3389/fonc.2019.00094
pmc: PMC6401644
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
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