CD133 suppresses neuroblastoma cell differentiation via signal pathway modification
CD133 (prominin-1) is a transmembrane glycoprotein expressed on the surface of normal and cancer stem cells (tumor-initiating cells), progenitor cells, rod photoreceptor cells and a variety of epithelial cells. Although CD133 is widely used as a marker of various somatic and putative cancer stem cel...
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| Veröffentlicht in: | Oncogene 2011-01, Vol.30 (1), p.97-105 |
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| creator | Takenobu, H Shimozato, O Nakamura, T Ochiai, H Yamaguchi, Y Ohira, M Nakagawara, A Kamijo, T |
| description | CD133 (prominin-1) is a transmembrane glycoprotein expressed on the surface of normal and cancer stem cells (tumor-initiating cells), progenitor cells, rod photoreceptor cells and a variety of epithelial cells. Although CD133 is widely used as a marker of various somatic and putative cancer stem cells, its contribution to the fundamental properties of cancer cells, such as tumorigenesis and differentiation, remains to be elucidated. In the present report, we found that CD133 was expressed in several neuroblastoma (NB) cell lines/tumor samples. Intriguingly, CD133 repressed NB cell differentiation, for example neurite extension and the expression of differentiation marker proteins, and was decreased by several differentiation stimuli, but accelerated cell proliferation, anchorage-independent colony formation and
in vivo
tumor formation of NB cells. NB cell line and primary tumor-sphere experiments indicated that the molecular mechanism of CD133-related differentiation suppression in NB was in part dependent on neurotrophic receptor RET tyrosine kinase regulation. RET transcription was suppressed by CD133 in NB cells and glial cell line-derived neurotrophic factor treatment failed to induce RET in CD133-expressing cells; RET overexpression rescued CD133-related inhibition of neurite elongation. Of note, CD133-related NB cell differentiation and RET repression were mainly dependent on p38MAPK and PI3K/Akt pathways. Furthermore, CD133 has a function in growth and RET expression in NB cell line- and primary tumor cell-derived tumor spheres. To the best of our knowledge, this is the first report of the function of CD133 in cancer cells and our findings may be applied to improve differentiation induction therapy for NB patients. |
| doi_str_mv | 10.1038/onc.2010.383 |
| format | Article |
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in vivo
tumor formation of NB cells. NB cell line and primary tumor-sphere experiments indicated that the molecular mechanism of CD133-related differentiation suppression in NB was in part dependent on neurotrophic receptor RET tyrosine kinase regulation. RET transcription was suppressed by CD133 in NB cells and glial cell line-derived neurotrophic factor treatment failed to induce RET in CD133-expressing cells; RET overexpression rescued CD133-related inhibition of neurite elongation. Of note, CD133-related NB cell differentiation and RET repression were mainly dependent on p38MAPK and PI3K/Akt pathways. Furthermore, CD133 has a function in growth and RET expression in NB cell line- and primary tumor cell-derived tumor spheres. To the best of our knowledge, this is the first report of the function of CD133 in cancer cells and our findings may be applied to improve differentiation induction therapy for NB patients.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2010.383</identifier><identifier>PMID: 20818439</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/136/142 ; 631/67/581 ; 631/80/86 ; 692/699/67/1922 ; AC133 Antigen ; Animals ; Antigens, CD - metabolism ; Apoptosis ; Biological and medical sciences ; Care and treatment ; Cell Biology ; Cell Differentiation - physiology ; Cell differentiation, maturation, development, hematopoiesis ; Cell Growth Processes - physiology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Fundamental and applied biological sciences. Psychology ; Genetic aspects ; Genetics ; Glycoproteins ; Glycoproteins - metabolism ; Health aspects ; HEK293 Cells ; Human Genetics ; Humans ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Mice, Nude ; Molecular and cellular biology ; Neuroblastoma ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; Neurology ; Oncology ; original-article ; Peptides - metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-ret - metabolism ; Signal Transduction ; Stem cells ; T cells ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Oncogene, 2011-01, Vol.30 (1), p.97-105</ispartof><rights>Macmillan Publishers Limited 2011</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2011 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 6, 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c547t-380f7d7a60822046076e3c73ee220e9f27834c9cc810a319b2848930d04dfe873</citedby><cites>FETCH-LOGICAL-c547t-380f7d7a60822046076e3c73ee220e9f27834c9cc810a319b2848930d04dfe873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2010.383$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2010.383$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2725,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23876618$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20818439$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takenobu, H</creatorcontrib><creatorcontrib>Shimozato, O</creatorcontrib><creatorcontrib>Nakamura, T</creatorcontrib><creatorcontrib>Ochiai, H</creatorcontrib><creatorcontrib>Yamaguchi, Y</creatorcontrib><creatorcontrib>Ohira, M</creatorcontrib><creatorcontrib>Nakagawara, A</creatorcontrib><creatorcontrib>Kamijo, T</creatorcontrib><title>CD133 suppresses neuroblastoma cell differentiation via signal pathway modification</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>CD133 (prominin-1) is a transmembrane glycoprotein expressed on the surface of normal and cancer stem cells (tumor-initiating cells), progenitor cells, rod photoreceptor cells and a variety of epithelial cells. Although CD133 is widely used as a marker of various somatic and putative cancer stem cells, its contribution to the fundamental properties of cancer cells, such as tumorigenesis and differentiation, remains to be elucidated. In the present report, we found that CD133 was expressed in several neuroblastoma (NB) cell lines/tumor samples. Intriguingly, CD133 repressed NB cell differentiation, for example neurite extension and the expression of differentiation marker proteins, and was decreased by several differentiation stimuli, but accelerated cell proliferation, anchorage-independent colony formation and
in vivo
tumor formation of NB cells. NB cell line and primary tumor-sphere experiments indicated that the molecular mechanism of CD133-related differentiation suppression in NB was in part dependent on neurotrophic receptor RET tyrosine kinase regulation. RET transcription was suppressed by CD133 in NB cells and glial cell line-derived neurotrophic factor treatment failed to induce RET in CD133-expressing cells; RET overexpression rescued CD133-related inhibition of neurite elongation. Of note, CD133-related NB cell differentiation and RET repression were mainly dependent on p38MAPK and PI3K/Akt pathways. Furthermore, CD133 has a function in growth and RET expression in NB cell line- and primary tumor cell-derived tumor spheres. To the best of our knowledge, this is the first report of the function of CD133 in cancer cells and our findings may be applied to improve differentiation induction therapy for NB patients.</description><subject>631/136/142</subject><subject>631/67/581</subject><subject>631/80/86</subject><subject>692/699/67/1922</subject><subject>AC133 Antigen</subject><subject>Animals</subject><subject>Antigens, CD - metabolism</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Cell Differentiation - physiology</subject><subject>Cell differentiation, maturation, development, hematopoiesis</subject><subject>Cell Growth Processes - physiology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic aspects</subject><subject>Genetics</subject><subject>Glycoproteins</subject><subject>Glycoproteins - metabolism</subject><subject>Health aspects</subject><subject>HEK293 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Molecular and cellular biology</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - metabolism</subject><subject>Neuroblastoma - pathology</subject><subject>Neurology</subject><subject>Oncology</subject><subject>original-article</subject><subject>Peptides - metabolism</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-ret - metabolism</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>T cells</subject><subject>Tumors of the nervous system. 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Although CD133 is widely used as a marker of various somatic and putative cancer stem cells, its contribution to the fundamental properties of cancer cells, such as tumorigenesis and differentiation, remains to be elucidated. In the present report, we found that CD133 was expressed in several neuroblastoma (NB) cell lines/tumor samples. Intriguingly, CD133 repressed NB cell differentiation, for example neurite extension and the expression of differentiation marker proteins, and was decreased by several differentiation stimuli, but accelerated cell proliferation, anchorage-independent colony formation and
in vivo
tumor formation of NB cells. NB cell line and primary tumor-sphere experiments indicated that the molecular mechanism of CD133-related differentiation suppression in NB was in part dependent on neurotrophic receptor RET tyrosine kinase regulation. RET transcription was suppressed by CD133 in NB cells and glial cell line-derived neurotrophic factor treatment failed to induce RET in CD133-expressing cells; RET overexpression rescued CD133-related inhibition of neurite elongation. Of note, CD133-related NB cell differentiation and RET repression were mainly dependent on p38MAPK and PI3K/Akt pathways. Furthermore, CD133 has a function in growth and RET expression in NB cell line- and primary tumor cell-derived tumor spheres. To the best of our knowledge, this is the first report of the function of CD133 in cancer cells and our findings may be applied to improve differentiation induction therapy for NB patients.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20818439</pmid><doi>10.1038/onc.2010.383</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/136/142 631/67/581 631/80/86 692/699/67/1922 AC133 Antigen Animals Antigens, CD - metabolism Apoptosis Biological and medical sciences Care and treatment Cell Biology Cell Differentiation - physiology Cell differentiation, maturation, development, hematopoiesis Cell Growth Processes - physiology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Fundamental and applied biological sciences. Psychology Genetic aspects Genetics Glycoproteins Glycoproteins - metabolism Health aspects HEK293 Cells Human Genetics Humans Internal Medicine Medical sciences Medicine Medicine & Public Health Mice Mice, Nude Molecular and cellular biology Neuroblastoma Neuroblastoma - metabolism Neuroblastoma - pathology Neurology Oncology original-article Peptides - metabolism Phosphorylation Proto-Oncogene Proteins c-ret - metabolism Signal Transduction Stem cells T cells Tumors of the nervous system. Phacomatoses |
| title | CD133 suppresses neuroblastoma cell differentiation via signal pathway modification |
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