The aryl hydrocarbon receptor-dependent disruption of contact inhibition in rat liver WB-F344 epithelial cells is linked with induction of survivin, but not with inhibition of apoptosis

0446223 - BFÚ 2016 RIV IE eng J - Journal Article
Svobodová, Jana - Kabátková, Markéta - Šmerdová, Lenka - Brenerová, P. - Dvořák, Z. - Machala, M. - Vondráček, Jan
The aryl hydrocarbon receptor-dependent disruption of contact inhibition in rat liver WB-F344 epithelial cells is linked with induction of survivin, but not with inhibition of apoptosis.
Toxicology. Roč. 333, JUL 2015 (2015), s. 37-44. ISSN 0300-483X
R&D Projects: GA ČR(CZ) GA13-07711S
Institutional support: RVO:68081707
Keywords : TUMOR PROMOTION * AH RECEPTOR * STEM-CELLS
Subject RIV: BO - Biophysics
Impact factor: 3.817, year: 2015

Inhibition of apoptosis by the ligands of the aryl hydrocarbon receptor (AhR) has been proposed to play a role in their tumor promoting effects on liver parenchymal cells. However, little is presently known about the impact of toxic AhR ligands, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on apoptosis in other liver cell types, such as in liver epithelial/progenitor cells. In the present study, we focused on the effects of TCDD on apoptosis regulation in a model of liver progenitor cells, rat WB-F344 cell line, during the TCDD-elicited release from contact inhibition. The stimulation of cell proliferation in this cell line was associated with deregulated expression of a number of genes known to be under transcriptional control of the Hippo signaling pathway, a principal regulatory pathway involved in contact inhibition of cell proliferation.
Permanent Link: http://hdl.handle.net/11104/0248216