Sphingosine-1-phosphate promotes expansion of cancer stem cells via S1PR3 by a ligand-independent Notch activation
Many tumours originate from cancer stem cells (CSCs), which is a small population of cells that display stem cell properties. However, the molecular mechanisms that regulate CSC frequency remain poorly understood. Here, using microarray screening in aldehyde dehydrogenase (ALDH)-positive CSC model,...
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| Veröffentlicht in: | Nature communications 2014-09, Vol.5 (1), p.4806-4806, Article 4806 |
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| creator | Hirata, Naoya Yamada, Shigeru Shoda, Takuji Kurihara, Masaaki Sekino, Yuko Kanda, Yasunari |
| description | Many tumours originate from cancer stem cells (CSCs), which is a small population of cells that display stem cell properties. However, the molecular mechanisms that regulate CSC frequency remain poorly understood. Here, using microarray screening in aldehyde dehydrogenase (ALDH)-positive CSC model, we identify a fundamental role for a lipid mediator sphingosine-1-phosphate (S1P) in CSC expansion. Stimulation with S1P enhances ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation. CSCs overexpressing sphingosine kinase 1 (SphK1), an S1P-producing enzyme, show increased ability to develop tumours in nude mice, compared with parent cells or CSCs. Tumorigenicity of CSCs overexpressing SphK1 is inhibited by
S1PR3
knockdown or S1PR3 antagonist. Breast cancer patient-derived mammospheres contain SphK1
+
/ALDH1
+
cells or S1PR3
+
/ALDH1
+
cells. Our findings provide new insights into the lipid-mediated regulation of CSCs via Notch signalling, and rationale for targeting S1PR3 in cancer.
Many tumours originate from cancer stem cells (CSCs), a small population of cells that display stem cell properties. Here Kanda and colleagues show that the lipid mediator, sphingosine-1 phosphate (S1P), enhances expansion of ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation, providing a rationale for targeting S1PR3 in cancer. |
| doi_str_mv | 10.1038/ncomms5806 |
| format | Article |
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S1PR3
knockdown or S1PR3 antagonist. Breast cancer patient-derived mammospheres contain SphK1
+
/ALDH1
+
cells or S1PR3
+
/ALDH1
+
cells. Our findings provide new insights into the lipid-mediated regulation of CSCs via Notch signalling, and rationale for targeting S1PR3 in cancer.
Many tumours originate from cancer stem cells (CSCs), a small population of cells that display stem cell properties. Here Kanda and colleagues show that the lipid mediator, sphingosine-1 phosphate (S1P), enhances expansion of ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation, providing a rationale for targeting S1PR3 in cancer.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms5806</identifier><identifier>PMID: 25254944</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/95 ; 631/67/71 ; 631/80/86 ; 96 ; 96/100 ; 96/31 ; 96/95 ; Animals ; Breast Neoplasms - enzymology ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - physiopathology ; Cell Line, Tumor ; Cell Proliferation ; Female ; Humanities and Social Sciences ; Humans ; Lysophospholipids - metabolism ; Mice ; Mice, Inbred BALB C ; multidisciplinary ; Neoplastic Stem Cells - cytology ; Neoplastic Stem Cells - metabolism ; Phosphotransferases (Alcohol Group Acceptor) - genetics ; Phosphotransferases (Alcohol Group Acceptor) - metabolism ; Receptors, Lysosphingolipid - genetics ; Receptors, Lysosphingolipid - metabolism ; Receptors, Notch - genetics ; Receptors, Notch - metabolism ; Science ; Science (multidisciplinary) ; Signal Transduction ; Sphingosine - analogs & derivatives ; Sphingosine - metabolism</subject><ispartof>Nature communications, 2014-09, Vol.5 (1), p.4806-4806, Article 4806</ispartof><rights>Springer Nature Limited 2014</rights><rights>Copyright Nature Publishing Group Sep 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-7da2f06ebb4902334f8da70e2a6fffa8945827ce6774cdd78177032393cd40f83</citedby><cites>FETCH-LOGICAL-c453t-7da2f06ebb4902334f8da70e2a6fffa8945827ce6774cdd78177032393cd40f83</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/ncomms5806$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://doi.org/10.1038/ncomms5806$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41099,42168,51554</link.rule.ids><linktorsrc>$$Uhttps://doi.org/10.1038/ncomms5806$$EView_record_in_Springer_Nature$$FView_record_in_$$GSpringer_Nature</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25254944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirata, Naoya</creatorcontrib><creatorcontrib>Yamada, Shigeru</creatorcontrib><creatorcontrib>Shoda, Takuji</creatorcontrib><creatorcontrib>Kurihara, Masaaki</creatorcontrib><creatorcontrib>Sekino, Yuko</creatorcontrib><creatorcontrib>Kanda, Yasunari</creatorcontrib><title>Sphingosine-1-phosphate promotes expansion of cancer stem cells via S1PR3 by a ligand-independent Notch activation</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Many tumours originate from cancer stem cells (CSCs), which is a small population of cells that display stem cell properties. However, the molecular mechanisms that regulate CSC frequency remain poorly understood. Here, using microarray screening in aldehyde dehydrogenase (ALDH)-positive CSC model, we identify a fundamental role for a lipid mediator sphingosine-1-phosphate (S1P) in CSC expansion. Stimulation with S1P enhances ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation. CSCs overexpressing sphingosine kinase 1 (SphK1), an S1P-producing enzyme, show increased ability to develop tumours in nude mice, compared with parent cells or CSCs. Tumorigenicity of CSCs overexpressing SphK1 is inhibited by
S1PR3
knockdown or S1PR3 antagonist. Breast cancer patient-derived mammospheres contain SphK1
+
/ALDH1
+
cells or S1PR3
+
/ALDH1
+
cells. Our findings provide new insights into the lipid-mediated regulation of CSCs via Notch signalling, and rationale for targeting S1PR3 in cancer.
Many tumours originate from cancer stem cells (CSCs), a small population of cells that display stem cell properties. Here Kanda and colleagues show that the lipid mediator, sphingosine-1 phosphate (S1P), enhances expansion of ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation, providing a rationale for targeting S1PR3 in cancer.</description><subject>13/95</subject><subject>631/67/71</subject><subject>631/80/86</subject><subject>96</subject><subject>96/100</subject><subject>96/31</subject><subject>96/95</subject><subject>Animals</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - physiopathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Female</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Lysophospholipids - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>multidisciplinary</subject><subject>Neoplastic Stem Cells - cytology</subject><subject>Neoplastic Stem Cells - 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Academic</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Hirata, Naoya</au><au>Yamada, Shigeru</au><au>Shoda, Takuji</au><au>Kurihara, Masaaki</au><au>Sekino, Yuko</au><au>Kanda, Yasunari</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sphingosine-1-phosphate promotes expansion of cancer stem cells via S1PR3 by a ligand-independent Notch activation</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2014-09-25</date><risdate>2014</risdate><volume>5</volume><issue>1</issue><spage>4806</spage><epage>4806</epage><pages>4806-4806</pages><artnum>4806</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Many tumours originate from cancer stem cells (CSCs), which is a small population of cells that display stem cell properties. However, the molecular mechanisms that regulate CSC frequency remain poorly understood. Here, using microarray screening in aldehyde dehydrogenase (ALDH)-positive CSC model, we identify a fundamental role for a lipid mediator sphingosine-1-phosphate (S1P) in CSC expansion. Stimulation with S1P enhances ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation. CSCs overexpressing sphingosine kinase 1 (SphK1), an S1P-producing enzyme, show increased ability to develop tumours in nude mice, compared with parent cells or CSCs. Tumorigenicity of CSCs overexpressing SphK1 is inhibited by
S1PR3
knockdown or S1PR3 antagonist. Breast cancer patient-derived mammospheres contain SphK1
+
/ALDH1
+
cells or S1PR3
+
/ALDH1
+
cells. Our findings provide new insights into the lipid-mediated regulation of CSCs via Notch signalling, and rationale for targeting S1PR3 in cancer.
Many tumours originate from cancer stem cells (CSCs), a small population of cells that display stem cell properties. Here Kanda and colleagues show that the lipid mediator, sphingosine-1 phosphate (S1P), enhances expansion of ALDH-positive CSCs via S1P receptor 3 (S1PR3) and subsequent Notch activation, providing a rationale for targeting S1PR3 in cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25254944</pmid><doi>10.1038/ncomms5806</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/95 631/67/71 631/80/86 96 96/100 96/31 96/95 Animals Breast Neoplasms - enzymology Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - physiopathology Cell Line, Tumor Cell Proliferation Female Humanities and Social Sciences Humans Lysophospholipids - metabolism Mice Mice, Inbred BALB C multidisciplinary Neoplastic Stem Cells - cytology Neoplastic Stem Cells - metabolism Phosphotransferases (Alcohol Group Acceptor) - genetics Phosphotransferases (Alcohol Group Acceptor) - metabolism Receptors, Lysosphingolipid - genetics Receptors, Lysosphingolipid - metabolism Receptors, Notch - genetics Receptors, Notch - metabolism Science Science (multidisciplinary) Signal Transduction Sphingosine - analogs & derivatives Sphingosine - metabolism |
| title | Sphingosine-1-phosphate promotes expansion of cancer stem cells via S1PR3 by a ligand-independent Notch activation |
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