2012
TGF-beta 1 signaling plays a dominant role in the crosstalk between TGF-beta 1 and the aryl hydrocarbon receptor ligand in prostate epithelial cells
STARŠÍCHOVÁ, Andrea; Eva HRUBÁ; Eva SLABÁKOVÁ; Zuzana PERNICOVÁ; Jiřina PROCHÁZKOVÁ et al.Základní údaje
Originální název
TGF-beta 1 signaling plays a dominant role in the crosstalk between TGF-beta 1 and the aryl hydrocarbon receptor ligand in prostate epithelial cells
Autoři
STARŠÍCHOVÁ, Andrea; Eva HRUBÁ; Eva SLABÁKOVÁ; Zuzana PERNICOVÁ; Jiřina PROCHÁZKOVÁ ORCID; Kateřina PĚNČÍKOVÁ; Václav ŠEDA ORCID; Markéta KABÁTKOVÁ; Jan VONDRÁČEK; Alois KOZUBÍK; Miroslav MACHALA a Karel SOUČEK
Vydání
Cellular Signalling, NEW YORK, ELSEVIER SCIENCE INC, 2012, 0898-6568
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
Genetika a molekulární biologie
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 4.304
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/12:00081842
Organizační jednotka
Přírodovědecká fakulta
UT WoS
Klíčová slova anglicky
Transforming growth factor-beta; Prostate epithelial cells; Aryl hydrocarbon receptor; SMAD4
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 25. 5. 2017 17:13, Ing. Nicole Zrilić
Anotace
V originále
Crosstalk between the aryl hydrocarbon receptor (AhR) and transforming growth factor-beta 1 (TGF-beta 1) signaling has been observed in various experimental models. However, both molecular mechanism underlying this crosstalk and tissue-specific context of this interaction are still only partially understood. In a model of human non-tumorigenic prostate epithelial cells BPH-1, derived from the benign prostatic hyperplasia, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) persistently activates the AhR signaling pathway and induces expression of xenobiotic metabolizing enzymes, such as CYP1A1 or CYP1B1. Here we demonstrate that TGF-beta 1 suppresses the AhR-mediated gene expression through multiple mechanisms, involving inhibition of AhR expression and down-regulation of nuclear AhR, via a SMAD4-dependent pathway. In contrast, TCDD-induced AhR signaling does not affect either TGF-beta 1-regulated gene expression or epithelial-to-mesenchymal transition. These observations suggest that, in the context of prostate epithelium, TGF-beta 1 signaling plays a dominant role in the crosstalk with AhR signaling pathway. Given the importance of TGF-beta 1 signaling in regulation of prostate epithelial tissue homeostasis, as well as the recently revealed role of AhR in prostate development and tumorigenesis, the above findings contribute to our understanding of the mechanisms underlying the crosstalk between the two signaling pathways in the prostate-specific context. (C) 2012 Elsevier Inc. All rights reserved.