Stable Transfection of U937 Cells with Sense or Antisense RXR-α cDNA Suggests a Role for RXR-α in the Control of Monoblastic Differentiation Induced by Retinoic Acid and Vitamin D

1997 ◽  
Vol 236 (1) ◽  
pp. 94-102 ◽  
Author(s):  
Timothy R.P. Brown ◽  
Timothy J. Stonehouse ◽  
Joel S. Branch ◽  
Paul M. Brickell ◽  
David R. Katz
Keyword(s):  
Vitamin D ◽  
Retinoic Acid ◽  
Stable Transfection ◽  
U937 Cells

VITAMIN D DERIVATIVES IN COMBINATION WITH 9-cis RETINOIC ACID PROMOTE ACTIVE CELL DEATH IN BREAST CANCER CELLS

1995 ◽  
Vol 14 (3) ◽  
pp. 391-394 ◽  
Author(s):  
S Y James ◽  
A G Mackay ◽  
K W Colston
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
P53 Protein ◽  
Protein A ◽  
Therapeutic Implications ◽  
Protein Levels ◽  
Mcf 7

ABSTRACT The effects of the novel vitamin D analogue, EB1089 alone, or in combination with the retinoid, 9-cis retinoic acid (9-cis RA) on indices of apoptosis in MCF-7 breast cancer cells have been examined. EB1089 was capable of reducing bcl-2 protein, a suppressor of apoptosis, and increasing p53 protein levels in MCF-7 cell cultures following 96h treatment. In the presence of 9-cis RA, EB1089 acted to further enhance the down-regulation and up-regulation of bcl-2 and p53 respectively. Furthermore, EB1089 induces DNA fragmentation in MCF-7 cells, a key feature of apoptosis, alone and in combination with 9-cis RA in situ. The observation that EB1089 and 9-cis RA act in a cooperative manner to enhance induction of apoptosis in these cells may have therapeutic implications.

Effects of vitamin D and retinoic acid on human glioblastoma cell lines

1995 ◽  
Vol 133 (3-4) ◽  
pp. 184-190 ◽  
Author(s):  
L. Magrassi ◽  
G. Butti ◽  
S. Pezzotta ◽  
L. Infuso ◽  
G. Milanesi
Keyword(s):  
Vitamin D ◽  
Retinoic Acid ◽  
Cell Lines ◽  
Glioblastoma Cell ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cell ◽  
Glioblastoma Cell Lines

scholarly journals Vitamin D interferes with transactivation of the growth hormone gene by thyroid hormone and retinoic acid.

1996 ◽  
Vol 16 (1) ◽  
pp. 318-327 ◽  
Author(s):  
P Garcia-Villalba ◽  
A M Jimenez-Lara ◽  
A Aranda
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Vitamin D Receptor ◽  
Growth Hormone Gene ◽  
Dependent Manner ◽  
Transcriptional Responses ◽  
Response Element

The thyroid hormone, retinoic acid (RA), and vitamin D regulate gene expression by binding to similar receptors which act as ligand-inducible transcription factors. Incubation of pituitary GH4C1 cells with nanomolar concentrations of vitamin D markedly reduces the response of the rat growth hormone mRNA to thyroid hormone triiodothyronine (T3) and RA. The stimulation of growth hormone gene expression by both ligands is mediated by a common hormone response element (TREGH) present in the 5'-flanking region of the gene, and the inhibition caused by vitamin D is due to transcriptional interference of the vitamin D receptor on this DNA element. No inhibition of the basal promoter activity by the vitamin was observed. The response to T3 and RA of a heterologous promoter containing this element, the palindromic T3- and RA-responsive sequence TREPAL, or a direct repeat of the same motif is also inhibited by vitamin D. In contrast, vitamin D strongly induces the activity of constructs containing a vitamin D response element, and neither T3 nor RA reduces vitamin D-mediated transactivation. Transfection with an expression vector for the retinoid X receptor alpha (RXR alpha) increases transactivation by T3 and RA but does not abolish the inhibition caused by the vitamin. Gel retardation experiments show that the vitamin D receptor (VDR) as a heterodimer with RXR weakly binds to the T3- and RA-responsive elements. Additionally, VDR displaces binding of T3 and RA receptors in a dose-dependent manner. Our data suggest the formation of TR-VDR and RAR-VDR heterodimers with RXR. The fact that the same response element mediates opposite effects of at least four different nuclear receptors provides a greater complexity and flexibility of the transcriptional responses to their ligands.

Sign in / Sign up

Export Citation Format

Share Document