Article
Refine
Year of publication
- 2017 (56) (remove)
Document Type
- Article (56) (remove)
Has Fulltext
- yes (56)
Is part of the Bibliography
- no (56)
Keywords
- - (54)
- barrier discharge (3)
- gap voltage (3)
- memory effect (3)
- surface charge (3)
- ALK5 (2)
- PAR2 (2)
- inductively coupled plasma (2)
- laser photodetachment (2)
- microwave interferometry (2)
Institute
- Institut für Physik (9)
- Institut für Botanik und Landschaftsökologie & Botanischer Garten (3)
- Institut für Community Medicine (3)
- Institut für Immunologie u. Transfusionsmedizin - Abteilung Transfusionsmedizin (3)
- Institut für Pharmakologie (3)
- Institut für Psychologie (3)
- Klinik und Poliklinik für Neurologie (3)
- Institut für Biochemie (2)
- Institut für Erziehungswissenschaft (2)
- Institut für Mikrobiologie - Abteilung für Genetik & Biochemie (2)
Publisher
- MDPI (15)
- S. Karger AG (15)
- Frontiers Media S.A. (14)
- IOP Publishing (9)
- De Gruyter (2)
The G protein-coupled receptor proteinase-activated receptor 2 (PAR2) has been implicated
in various aspects of cellular physiology including inflammation, obesity and cancer. In cancer,
it usually acts as a driver of cancer progression in various tumor types by promoting invasion and
metastasis in response to activation by serine proteinases. Recently, we discovered another mode
through which PAR2 may enhance tumorigenesis: crosstalk with transforming growth factor-β
(TGF-β) signaling to promote TGF-β1-induced cell migration/invasion and invasion-associated gene
expression in ductal pancreatic adenocarcinoma (PDAC) cells. In this chapter, we review what is
known about the cellular TGF-β responses and signaling pathways affected by PAR2 expression,
the signaling activities of PAR2 required for promoting TGF-β signaling, and the potential molecular
mechanism(s) that underlie(s) the TGF-β signaling–promoting effect. Since PAR2 is activated through
various serine proteinases and biased agonists, it may couple TGF-β signaling to a diverse range of
other physiological processes that may or may not predispose cells to cancer development such as
local inflammation, systemic coagulation and pathogen infection.