Limits...
Involvement of COUP-TFs in Cancer Progression.

Boudot A, Le Dily F, Pakdel F - Cancers (Basel) (2011)

Bottom Line: Although COUP-TFs are expressed in a wide range of tissues in adults, little is known about their functions at later stages of development or in organism homeostasis.COUP-TFs are expressed in cancer cell lines of various origins and increasing studies suggest they play roles in cell fate determination and, potentially, in cancer progression.Nevertheless, the exact roles of COUP-TFs in these processes remain unclear and even controversial.

View Article: PubMed Central - PubMed

Affiliation: Molecular and Cellular Interactions, UMR CNRS 6026, IFR 140 GFSA, University of Rennes 1, Rennes, France. farzad.pakdel@univ-rennes1.fr.

ABSTRACT
The orphan receptors COUP-TFI and COUP-TFII are members of the nuclear receptor superfamily that play distinct and critical roles in vertebrate organogenesis, as demonstrated by loss-of-function COUP-TFI and/or COUP-TFII mutant mice. Although COUP-TFs are expressed in a wide range of tissues in adults, little is known about their functions at later stages of development or in organism homeostasis. COUP-TFs are expressed in cancer cell lines of various origins and increasing studies suggest they play roles in cell fate determination and, potentially, in cancer progression. Nevertheless, the exact roles of COUP-TFs in these processes remain unclear and even controversial. In this review, we report both in vitro and in vivo data describing known and suspected actions of COUP-TFs that suggest that these factors are involved in modification of the phenotype of cancer cells, notably of epithelial origin.

No MeSH data available.


Related in: MedlinePlus

Identified-targets of COUP-TFs described in cancer progression or regression. COUP-TFs regulate positively (+) or negatively (−) the expression of various target genes or signaling pathways that could influence proliferation, survival or migration of cancer cells as well as differentiation state or angiogenesis of tumors. These contributions are linked to cancer progression (A) or cancer regression (B). MMP-2, matrix-metalo-protease-2; VEGF, vascular endothelial growth factor; RA, retinoic acid; ERα, estrogen receptor alpha; PR, progesterone receptor; Bcl2, B-cell CLL/lymphoma 2; RARβ, retinoic acid receptor beta; AP-1, activator protein-1; P21, cyclin-dependent kinase inhibitor 1A.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3756385&req=5

f3-cancers-03-00700: Identified-targets of COUP-TFs described in cancer progression or regression. COUP-TFs regulate positively (+) or negatively (−) the expression of various target genes or signaling pathways that could influence proliferation, survival or migration of cancer cells as well as differentiation state or angiogenesis of tumors. These contributions are linked to cancer progression (A) or cancer regression (B). MMP-2, matrix-metalo-protease-2; VEGF, vascular endothelial growth factor; RA, retinoic acid; ERα, estrogen receptor alpha; PR, progesterone receptor; Bcl2, B-cell CLL/lymphoma 2; RARβ, retinoic acid receptor beta; AP-1, activator protein-1; P21, cyclin-dependent kinase inhibitor 1A.

Mentions: Several studies have analyzed the influence of orphan NRs on cancer cell phenotype and their potential involvement in cancer progression, modifications of cellular signaling pathways and cell response to treatments. Particularly, one of the principal actions of COUP-TFs may be the regulation of the activity of liganded NRs such as ER and RAR in the control of cell growth in hormone-dependent tumors. Depending on the cell type and the biological processes studied, COUP-TFs have been proposed to act positively or negatively on cancer progression (Figure 3). Notably, several studies suggest that, in line with their roles in cell fate determination, COUP-TFs can be involved in epithelio-mesenchymal transition, which is a critical event during oncogenesis. However, the exact role of COUP-TFs in generating the phenotype of cancer cells remains controversial.


Involvement of COUP-TFs in Cancer Progression.

Boudot A, Le Dily F, Pakdel F - Cancers (Basel) (2011)

Identified-targets of COUP-TFs described in cancer progression or regression. COUP-TFs regulate positively (+) or negatively (−) the expression of various target genes or signaling pathways that could influence proliferation, survival or migration of cancer cells as well as differentiation state or angiogenesis of tumors. These contributions are linked to cancer progression (A) or cancer regression (B). MMP-2, matrix-metalo-protease-2; VEGF, vascular endothelial growth factor; RA, retinoic acid; ERα, estrogen receptor alpha; PR, progesterone receptor; Bcl2, B-cell CLL/lymphoma 2; RARβ, retinoic acid receptor beta; AP-1, activator protein-1; P21, cyclin-dependent kinase inhibitor 1A.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756385&req=5

f3-cancers-03-00700: Identified-targets of COUP-TFs described in cancer progression or regression. COUP-TFs regulate positively (+) or negatively (−) the expression of various target genes or signaling pathways that could influence proliferation, survival or migration of cancer cells as well as differentiation state or angiogenesis of tumors. These contributions are linked to cancer progression (A) or cancer regression (B). MMP-2, matrix-metalo-protease-2; VEGF, vascular endothelial growth factor; RA, retinoic acid; ERα, estrogen receptor alpha; PR, progesterone receptor; Bcl2, B-cell CLL/lymphoma 2; RARβ, retinoic acid receptor beta; AP-1, activator protein-1; P21, cyclin-dependent kinase inhibitor 1A.
Mentions: Several studies have analyzed the influence of orphan NRs on cancer cell phenotype and their potential involvement in cancer progression, modifications of cellular signaling pathways and cell response to treatments. Particularly, one of the principal actions of COUP-TFs may be the regulation of the activity of liganded NRs such as ER and RAR in the control of cell growth in hormone-dependent tumors. Depending on the cell type and the biological processes studied, COUP-TFs have been proposed to act positively or negatively on cancer progression (Figure 3). Notably, several studies suggest that, in line with their roles in cell fate determination, COUP-TFs can be involved in epithelio-mesenchymal transition, which is a critical event during oncogenesis. However, the exact role of COUP-TFs in generating the phenotype of cancer cells remains controversial.

Bottom Line: Although COUP-TFs are expressed in a wide range of tissues in adults, little is known about their functions at later stages of development or in organism homeostasis.COUP-TFs are expressed in cancer cell lines of various origins and increasing studies suggest they play roles in cell fate determination and, potentially, in cancer progression.Nevertheless, the exact roles of COUP-TFs in these processes remain unclear and even controversial.

View Article: PubMed Central - PubMed

Affiliation: Molecular and Cellular Interactions, UMR CNRS 6026, IFR 140 GFSA, University of Rennes 1, Rennes, France. farzad.pakdel@univ-rennes1.fr.

ABSTRACT
The orphan receptors COUP-TFI and COUP-TFII are members of the nuclear receptor superfamily that play distinct and critical roles in vertebrate organogenesis, as demonstrated by loss-of-function COUP-TFI and/or COUP-TFII mutant mice. Although COUP-TFs are expressed in a wide range of tissues in adults, little is known about their functions at later stages of development or in organism homeostasis. COUP-TFs are expressed in cancer cell lines of various origins and increasing studies suggest they play roles in cell fate determination and, potentially, in cancer progression. Nevertheless, the exact roles of COUP-TFs in these processes remain unclear and even controversial. In this review, we report both in vitro and in vivo data describing known and suspected actions of COUP-TFs that suggest that these factors are involved in modification of the phenotype of cancer cells, notably of epithelial origin.

No MeSH data available.


Related in: MedlinePlus