| '''Chemokine (C-X-C motif) ligand 3''' (CXCL3) is a small [[cytokine]] belonging to the CXC [[chemokine]] family that is also known as ''GRO3 oncogene'' (GRO3), ''GRO protein gamma'' (GROg) and ''macrophage inflammatory protein-2-beta'' (MIP2b). CXCL3 controls [[chemotaxis|migration]] and [[cell adhesion|adhesion]] of [[monocyte]]s and mediates its effects on its target cell by interacting with a cell surface [[chemokine receptor]] called [[CXC chemokine receptors#CXCR1 and CXCR2|CXCR2]].<ref name="pmid15937099">{{cite journal | vauthors = Smith DF, Galkina E, Ley K, Huo Y | title = GRO family chemokines are specialized for monocyte arrest from flow | journal = Am. J. Physiol. Heart Circ. Physiol. | volume = 289 | issue = 5 | pages = H1976–84 |date=November 2005 | pmid = 15937099 | doi = 10.1152/ajpheart.00153.2005 }}</ref><ref name="pmid8702798">{{cite journal | vauthors = Ahuja SK, Murphy PM | title = The CXC chemokines growth-regulated oncogene (GRO) alpha, GRObeta, GROgamma, neutrophil-activating peptide-2, and epithelial cell-derived neutrophil-activating peptide-78 are potent agonists for the type B, but not the type A, human interleukin-8 receptor | journal = J. Biol. Chem. | volume = 271 | issue = 34 | pages = 20545–50 |date=August 1996 | pmid = 8702798 | doi = 10.1074/jbc.271.34.20545 }}</ref> More recently, it has been shown that Cxcl3 regulates cell autonomously the migration of the precursors of cerebellar granule neurons toward the internal layers of cerebellum, during the morphogenesis of [[cerebellum]].<ref name="pmid23115191">{{Cite journal | vauthors =Farioli-Vecchioli S, Cinà I, Ceccarelli M, Micheli L, Leonardi L, Ciotti MT, De Bardi M, Di Rocco C, Pallini R, Cavallaro S, Tirone F | title = Tis21 knock-out enhances the frequency of medulloblastoma in patched1 heterozygous mice by inhibiting the cxcl3-dependent migration of cerebellar neurons | journal = [[The Journal of Neuroscience]] | volume = 32 | issue = 44 | pages = 15547–15564 |date=October 2012 | doi = 10.1523/JNEUROSCI.0412-12.2012 | pmid = 23115191 }}</ref> Moreover, if the expression of Cxcl3 is reduced in cerebellar granule neuron precursors, this highly enhances the frequency of the medulloblastoma, the tumor of cerebellum. In fact, the reduced expression of Cxcl3 forces the cerebellar granule neuron precursors to remain at the surface of the cerebellum, where they highly proliferate under the stimulus of [[Sonic hedgehog]], becoming target of transforming insults. Remarkably, the treatment with CXCL3 completely prevents the growth of medulloblastoma lesions in a Shh-type mouse model of medulloblastoma.<ref>{{Cite journal | author = [[Ceccarelli M]], [[Micheli L]] & [[Tirone F]] | title = Suppression of Medulloblastoma Lesions by Forced Migration of Preneoplastic Precursor Cells with Intracerebellar Administration of the Chemokine Cxcl3 | journal = [[Frontiers in Pharmacology]] | volume = 7 | pages = 484 | year = 2016 | doi = 10.3389/fphar.2016.00484 | pmid = 28018222 | url =http://journal.frontiersin.org/article/10.3389/fphar.2016.00484/full}}</ref> Thus, CXCL3 is a target for medulloblastoma therapy. Cxcl3 is directly regulated transcriptionally by [[BTG2]] <ref name="pmid23115191"/> | | '''Chemokine (C-X-C motif) ligand 3''' (CXCL3) is a small [[cytokine]] belonging to the CXC [[chemokine]] family that is also known as ''GRO3 oncogene'' (GRO3), ''GRO protein gamma'' (GROg) and ''macrophage inflammatory protein-2-beta'' (MIP2b). CXCL3 controls [[chemotaxis|migration]] and [[cell adhesion|adhesion]] of [[monocyte]]s and mediates its effects on its target cell by interacting with a cell surface [[chemokine receptor]] called [[CXC chemokine receptors#CXCR1 and CXCR2|CXCR2]].<ref name="pmid15937099">{{cite journal | vauthors = Smith DF, Galkina E, Ley K, Huo Y | title = GRO family chemokines are specialized for monocyte arrest from flow | journal = Am. J. Physiol. Heart Circ. Physiol. | volume = 289 | issue = 5 | pages = H1976–84 |date=November 2005 | pmid = 15937099 | doi = 10.1152/ajpheart.00153.2005 }}</ref><ref name="pmid8702798">{{cite journal | vauthors = Ahuja SK, Murphy PM | title = The CXC chemokines growth-regulated oncogene (GRO) alpha, GRObeta, GROgamma, neutrophil-activating peptide-2, and epithelial cell-derived neutrophil-activating peptide-78 are potent agonists for the type B, but not the type A, human interleukin-8 receptor | journal = J. Biol. Chem. | volume = 271 | issue = 34 | pages = 20545–50 |date=August 1996 | pmid = 8702798 | doi = 10.1074/jbc.271.34.20545 }}</ref> More recently, it has been shown that Cxcl3 regulates cell autonomously the migration of the precursors of cerebellar granule neurons toward the internal layers of cerebellum, during the morphogenesis of [[cerebellum]].<ref name="pmid23115191">{{Cite journal | vauthors =Farioli-Vecchioli S, Cinà I, Ceccarelli M, Micheli L, Leonardi L, Ciotti MT, De Bardi M, Di Rocco C, Pallini R, Cavallaro S, Tirone F | title = Tis21 knock-out enhances the frequency of medulloblastoma in patched1 heterozygous mice by inhibiting the cxcl3-dependent migration of cerebellar neurons | journal = [[The Journal of Neuroscience]] | volume = 32 | issue = 44 | pages = 15547–15564 |date=October 2012 | doi = 10.1523/JNEUROSCI.0412-12.2012 | pmid = 23115191 }}</ref> Moreover, if the expression of Cxcl3 is reduced in cerebellar granule neuron precursors, this highly enhances the frequency of the medulloblastoma, the tumor of cerebellum. In fact, the reduced expression of Cxcl3 forces the cerebellar granule neuron precursors to remain at the surface of the cerebellum, where they highly proliferate under the stimulus of [[Sonic hedgehog]], becoming target of transforming insults. Remarkably, the treatment with CXCL3 completely prevents the growth of medulloblastoma lesions in a Shh-type mouse model of medulloblastoma.<ref>{{Cite journal | author = [[Ceccarelli M]], [[Micheli L]] & [[Tirone F]] | title = Suppression of Medulloblastoma Lesions by Forced Migration of Preneoplastic Precursor Cells with Intracerebellar Administration of the Chemokine Cxcl3 | journal = [[Frontiers in Pharmacology]] | volume = 7 | pages = 484 | year = 2016 | doi = 10.3389/fphar.2016.00484 | pmid = 28018222 | url =http://journal.frontiersin.org/article/10.3389/fphar.2016.00484/full | pmc=5159413}}</ref> Thus, CXCL3 is a target for medulloblastoma therapy. Cxcl3 is directly regulated transcriptionally by [[BTG2]] <ref name="pmid23115191"/> |
