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Sodium butyrate/retinoic acid costimulation induces apoptosis-independent growth arrest and cell differentiation in normal and ras-transformed seminal vesicle epithelial cells unresponsive to retinoic acid

Authors :
Daniela Pasquali
Francesco Morelli
Antonio Agostino Sinisi
Antonio Bellastella
S Metafora
Elisabetta Buommino
Buommino, Elisabetta
Pasquali, D
Sinisi, A. A
Bellastella, A
Morelli, F
Metafora, S.
Pasquali, Daniela
Sinisi, Aa
Source :
Journal of molecular endocrinology. 24(1)
Publication Year :
2000

Abstract

Retinoic acid (RA) and sodium butyrate (NaB) are regulators of cell growth and differentiation. We studied their effect on normal (SVC1) or v-Ki-ras-transformed (Ki-SVC1) rat seminal vesicle (SV) epithelial cell lines. The treatment of these cells with 10(-((7( M RA did not produce significant changes in the morphological and biochemical parameters analyzed. When RA was used in combination with 2 mM NaB, the treatment induced substantial morphological changes, apoptosis-independent growth arrest, up-regulation of tissue transglutaminase (tTGase), and down-regulation of beta and gamma RA receptor (RAR) mRNA expression. The same cells did not express RAR alpha either before or after NaB/RA treatment. A similar treatment did not change the amount of mRNA coding for the protein SV-IV (a typical differentiation marker of the SV epithelium) in normal or ras-transformed cells nor the level of v-Ki-ras mRNA in Ki-SVC1 cells. These findings suggest that a defective RA/RARs signaling pathway is probably the biochemical condition that underlies the unresponsiveness to RA of our in vitro culture system, and indirectly points to the possibility that the NaB/RA-induced effects were brought about by a cooperation at the transcription level between the histone deacetylase inhibitory activity of NaB and the ability of RA/RAR to modulate the expression of various genes involved in the control of cell growth and differentiation.

Details

ISSN :
09525041
Volume :
24
Issue :
1
Database :
OpenAIRE
Journal :
Journal of molecular endocrinology
Accession number :
edsair.doi.dedup.....7fa591792b15b30c64eeaa4678e8b1d0