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NFAT transcription factors are implicated in [[breast cancer]], more specifically in the process of cell motility at the basis of metastasis formation. Indeed, NFAT1 (NFATC2) is pro-invasive and pro-migratory in breast carcinoma.<ref name="pmid12080349">{{cite journal | vauthors = Jauliac S, López-Rodriguez C, Shaw LM, Brown LF, Rao A, Toker A | title = The role of NFAT transcription factors in integrin-mediated carcinoma invasion | journal = Nature Cell Biology | volume = 4 | issue = 7 | pages = 540–4 | date = Jul 2002 | pmid = 12080349 | doi = 10.1038/ncb816 }}</ref><ref name="pmid16307918">{{cite journal | vauthors = Yoeli-Lerner M, Yiu GK, Rabinovitz I, Erhardt P, Jauliac S, Toker A | title = Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT | journal = Molecular Cell | volume = 20 | issue = 4 | pages = 539–50 | date = Nov 2005 | pmid = 16307918 | doi = 10.1016/j.molcel.2005.10.033 }}</ref>
NFAT transcription factors are implicated in [[breast cancer]], more specifically in the process of cell motility at the basis of metastasis formation. Indeed, NFAT1 (NFATC2) is pro-invasive and pro-migratory in breast carcinoma.<ref name="pmid12080349">{{cite journal | vauthors = Jauliac S, López-Rodriguez C, Shaw LM, Brown LF, Rao A, Toker A | title = The role of NFAT transcription factors in integrin-mediated carcinoma invasion | journal = Nature Cell Biology | volume = 4 | issue = 7 | pages = 540–4 | date = Jul 2002 | pmid = 12080349 | doi = 10.1038/ncb816 }}</ref><ref name="pmid16307918">{{cite journal | vauthors = Yoeli-Lerner M, Yiu GK, Rabinovitz I, Erhardt P, Jauliac S, Toker A | title = Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT | journal = Molecular Cell | volume = 20 | issue = 4 | pages = 539–50 | date = Nov 2005 | pmid = 16307918 | doi = 10.1016/j.molcel.2005.10.033 }}</ref>


To increase cell motility NFAT1 up-regulates the gene of the [[LCN2|Lipocalin 2]] expression and modulate the TWEAKR/TWEAK axis.<ref name="pmid22767506">{{cite journal | vauthors = Gaudineau B, Fougère M, Guaddachi F, Lemoine F, de la Grange P, Jauliac S | title = Lipocalin 2, the TNF-like receptor TWEAKR and its ligand TWEAK act downstream of NFAT1 to regulate breast cancer cell invasion | journal = Journal of Cell Science | volume = 125 | issue = Pt 19 | pages = 4475–86 | date = Oct 2012 | pmid = 22767506 | doi = 10.1242/jcs.099879 }}</ref>
To increase cell motility NFAT1 up-regulates the gene of the [[LCN2|Lipocalin 2]] expression and modulate the TWEAKR/TWEAK axis.<ref name="pmid22767506">{{cite journal | vauthors = Gaudineau B, Fougère M, Guaddachi F, Lemoine F, de la Grange P, Jauliac S | title = Lipocalin 2, the TNF-like receptor TWEAKR and its ligand TWEAK act downstream of NFAT1 to regulate breast cancer cell invasion | journal = Journal of Cell Science | volume = 125 | issue = Pt 19 | pages = 4475–86 | date = Oct 2012 | pmid = 22767506 | doi = 10.1242/jcs.099879 | url = http://www.hal.inserm.fr/docs/00/71/58/76/PDF/jcs.099879.full.pdf }}</ref>


Translocation forming an in frame fusions product between [[Ewing sarcoma breakpoint region 1|EWSR1 gene]] and the NFATc2 gene has been described in bone tumor with a Ewing sarcoma-like clinical appearance. The translocation breakpoint led to the loss of the controlling elements of the NFATc2 protein and the fusion of the N terminal region of the EWSR1 gene conferred constant activation of the protein.<ref name="pmid19318479">{{cite journal | vauthors = Szuhai K, Ijszenga M, de Jong D, Karseladze A, Tanke HJ, Hogendoorn PC | title = The NFATc2 gene is involved in a novel cloned translocation in a Ewing sarcoma variant that couples its function in immunology to oncology | journal = Clinical Cancer Research | volume = 15 | issue = 7 | pages = 2259–68 | date = Apr 2009 | pmid = 19318479 | doi = 10.1158/1078-0432.CCR-08-2184 }}</ref>
Translocation forming an in frame fusions product between [[Ewing sarcoma breakpoint region 1|EWSR1 gene]] and the NFATc2 gene has been described in bone tumor with a Ewing sarcoma-like clinical appearance. The translocation breakpoint led to the loss of the controlling elements of the NFATc2 protein and the fusion of the N terminal region of the EWSR1 gene conferred constant activation of the protein.<ref name="pmid19318479">{{cite journal | vauthors = Szuhai K, Ijszenga M, de Jong D, Karseladze A, Tanke HJ, Hogendoorn PC | title = The NFATc2 gene is involved in a novel cloned translocation in a Ewing sarcoma variant that couples its function in immunology to oncology | journal = Clinical Cancer Research | volume = 15 | issue = 7 | pages = 2259–68 | date = Apr 2009 | pmid = 19318479 | doi = 10.1158/1078-0432.CCR-08-2184 }}</ref>
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* {{cite journal | vauthors = Horsley V, Pavlath GK | title = NFAT: ubiquitous regulator of cell differentiation and adaptation | journal = The Journal of Cell Biology | volume = 156 | issue = 5 | pages = 771–774 | date = Mar 2002 | pmid = 11877454 | pmc = 2173310 | doi = 10.1083/jcb.200111073 }}
* {{cite journal | vauthors = Horsley V, Pavlath GK | title = NFAT: ubiquitous regulator of cell differentiation and adaptation | journal = The Journal of Cell Biology | volume = 156 | issue = 5 | pages = 771–774 | date = Mar 2002 | pmid = 11877454 | pmc = 2173310 | doi = 10.1083/jcb.200111073 }}
* {{cite journal | vauthors = Aramburu J, Azzoni L, Rao A, Perussia B | title = Activation and expression of the nuclear factors of activated T cells, NFATp and NFATc, in human natural killer cells: regulation upon CD16 ligand binding | journal = The Journal of Experimental Medicine | volume = 182 | issue = 3 | pages = 801–810 | date = Sep 1995 | pmid = 7650486 | pmc = 2192167 | doi = 10.1084/jem.182.3.801 }}
* {{cite journal | vauthors = Aramburu J, Azzoni L, Rao A, Perussia B | title = Activation and expression of the nuclear factors of activated T cells, NFATp and NFATc, in human natural killer cells: regulation upon CD16 ligand binding | journal = The Journal of Experimental Medicine | volume = 182 | issue = 3 | pages = 801–810 | date = Sep 1995 | pmid = 7650486 | pmc = 2192167 | doi = 10.1084/jem.182.3.801 }}
* {{cite journal | vauthors = Auffray C, Behar G, Bois F, Bouchier C, Da Silva C, Devignes MD, Duprat S, Houlgatte R, Jumeau MN, Lamy B | title = [IMAGE: molecular integration of the analysis of the human genome and its expression] | journal = Comptes Rendus De L'Académie Des Sciences. Série III, Sciences De La Vie | volume = 318 | issue = 2 | pages = 263–72 | date = Feb 1995 | pmid = 7757816 | doi =  }}
* {{cite journal | vauthors = Auffray C, Behar G, Bois F, Bouchier C, Da Silva C, Devignes MD, Duprat S, Houlgatte R, Jumeau MN, Lamy B | title = [IMAGE: molecular integration of the analysis of the human genome and its expression] | journal = Comptes Rendus de l'Académie des Sciences, Série III | volume = 318 | issue = 2 | pages = 263–72 | date = Feb 1995 | pmid = 7757816 | doi =  }}
* {{cite journal | vauthors = Li X, Ho SN, Luna J, Giacalone J, Thomas DJ, Timmerman LA, Crabtree GR, Francke U | title = Cloning and chromosomal localization of the human and murine genes for the T-cell transcription factors NFATc and NFATp | journal = Cytogenetics and Cell Genetics | volume = 68 | issue = 3-4 | pages = 185–191 | year = 1995 | pmid = 7842733 | doi = 10.1159/000133910 }}
* {{cite journal | vauthors = Li X, Ho SN, Luna J, Giacalone J, Thomas DJ, Timmerman LA, Crabtree GR, Francke U | title = Cloning and chromosomal localization of the human and murine genes for the T-cell transcription factors NFATc and NFATp | journal = Cytogenetics and Cell Genetics | volume = 68 | issue = 3-4 | pages = 185–191 | year = 1995 | pmid = 7842733 | doi = 10.1159/000133910 }}
* {{cite journal | vauthors = Ho S, Timmerman L, Northrop J, Crabtree GR | title = Cloning and characterization of NF-ATc and NF-ATp: the cytoplasmic components of NF-AT | journal = Advances in Experimental Medicine and Biology | volume = 365 | issue =  | pages = 167–73 | year = 1995 | pmid = 7887301 | doi = 10.1007/978-1-4899-0987-9_17 }}
* {{cite journal | vauthors = Ho S, Timmerman L, Northrop J, Crabtree GR | title = Cloning and characterization of NF-ATc and NF-ATp: the cytoplasmic components of NF-AT | journal = Advances in Experimental Medicine and Biology | volume = 365 | issue =  | pages = 167–73 | year = 1995 | pmid = 7887301 | doi = 10.1007/978-1-4899-0987-9_17 }}

Revision as of 01:04, 24 October 2018

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Nuclear factor of activated T-cells, cytoplasmic 2 is a protein that in humans is encoded by the NFATC2 gene.[1]

Function

This gene is a member of the nuclear factor of activated T cells (NFAT) family. The product of this gene is a DNA-binding protein with a REL-homology region (RHR) and an NFAT-homology region (NHR). This protein is present in the cytosol and only translocates to the nucleus upon T cell receptor (TCR) stimulation, where it becomes a member of the nuclear factors of activated T cells transcription complex. This complex plays a central role in inducing gene transcription during the immune response. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.[2]

Clinical significance

NFAT transcription factors are implicated in breast cancer, more specifically in the process of cell motility at the basis of metastasis formation. Indeed, NFAT1 (NFATC2) is pro-invasive and pro-migratory in breast carcinoma.[3][4]

To increase cell motility NFAT1 up-regulates the gene of the Lipocalin 2 expression and modulate the TWEAKR/TWEAK axis.[5]

Translocation forming an in frame fusions product between EWSR1 gene and the NFATc2 gene has been described in bone tumor with a Ewing sarcoma-like clinical appearance. The translocation breakpoint led to the loss of the controlling elements of the NFATc2 protein and the fusion of the N terminal region of the EWSR1 gene conferred constant activation of the protein.[6]

Interactions

NFATC2 has been shown to interact with MEF2D,[7] EP300,[8] IRF4[9] and Protein kinase Mζ.[10]

References

  1. ↑ Northrop JP, Ho SN, Chen L, Thomas DJ, Timmerman LA, Nolan GP, Admon A, Crabtree GR (Jun 1994). "NF-AT components define a family of transcription factors targeted in T-cell activation". Nature. 369 (6480): 497–502. doi:10.1038/369497a0. PMID 8202141.
  2. ↑ "Entrez Gene: NFATC2 nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 2".
  3. ↑ Jauliac S, López-Rodriguez C, Shaw LM, Brown LF, Rao A, Toker A (Jul 2002). "The role of NFAT transcription factors in integrin-mediated carcinoma invasion". Nature Cell Biology. 4 (7): 540–4. doi:10.1038/ncb816. PMID 12080349.
  4. ↑ Yoeli-Lerner M, Yiu GK, Rabinovitz I, Erhardt P, Jauliac S, Toker A (Nov 2005). "Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT". Molecular Cell. 20 (4): 539–50. doi:10.1016/j.molcel.2005.10.033. PMID 16307918.
  5. ↑ Gaudineau B, Fougère M, Guaddachi F, Lemoine F, de la Grange P, Jauliac S (Oct 2012). "Lipocalin 2, the TNF-like receptor TWEAKR and its ligand TWEAK act downstream of NFAT1 to regulate breast cancer cell invasion" (PDF). Journal of Cell Science. 125 (Pt 19): 4475–86. doi:10.1242/jcs.099879. PMID 22767506.
  6. ↑ Szuhai K, Ijszenga M, de Jong D, Karseladze A, Tanke HJ, Hogendoorn PC (Apr 2009). "The NFATc2 gene is involved in a novel cloned translocation in a Ewing sarcoma variant that couples its function in immunology to oncology". Clinical Cancer Research. 15 (7): 2259–68. doi:10.1158/1078-0432.CCR-08-2184. PMID 19318479.
  7. ↑ Youn HD, Chatila TA, Liu JO (Aug 2000). "Integration of calcineurin and MEF2 signals by the coactivator p300 during T-cell apoptosis". The EMBO Journal. 19 (16): 4323–31. doi:10.1093/emboj/19.16.4323. PMC 302027. PMID 10944115.
  8. ↑ García-Rodríguez C, Rao A (Jun 1998). "Nuclear factor of activated T cells (NFAT)-dependent transactivation regulated by the coactivators p300/CREB-binding protein (CBP)". The Journal of Experimental Medicine. 187 (12): 2031–6. doi:10.1084/jem.187.12.2031. PMC 2212364. PMID 9625762.
  9. ↑ Rengarajan J, Mowen KA, McBride KD, Smith ED, Singh H, Glimcher LH (Apr 2002). "Interferon regulatory factor 4 (IRF4) interacts with NFATc2 to modulate interleukin 4 gene expression". The Journal of Experimental Medicine. 195 (8): 1003–12. doi:10.1084/jem.20011128. PMC 2193700. PMID 11956291.
  10. ↑ San-Antonio B, Iñiguez MA, Fresno M (Jul 2002). "Protein kinase Czeta phosphorylates nuclear factor of activated T cells and regulates its transactivating activity". The Journal of Biological Chemistry. 277 (30): 27073–80. doi:10.1074/jbc.M106983200. PMID 12021260.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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