NeuroD1 promotes neuroblastoma cell growth by inducing the expression of ALK
Neuroblastoma is derived from the sympathetic neuronal lineage of neural crest cells, and is the most frequently observed of the extracranial pediatric solid tumors. The neuronal differentiation factor, NeuroD1, has previously been shown to promote cell motility in neuroblastoma by suppressing the e...
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description | Neuroblastoma is derived from the sympathetic neuronal lineage of neural crest cells, and is the most frequently observed of the extracranial pediatric solid tumors. The neuronal differentiation factor, NeuroD1, has previously been shown to promote cell motility in neuroblastoma by suppressing the expression of Slit2. Here we report that NeuroD1 is also involved in the proliferation of neuroblastoma cells, including human cell lines and primary tumorspheres cultured from the tumor tissues of model mice. Interestingly, the growth inhibition of neuroblastoma cells induced by knockdown of NeuroD1 was accompanied by a reduction of ALK expression. ALK is known to be one of the important predisposition genes for neuroblastoma. The phenotype resulting from knockdown of NeuroD1 was suppressed by forced expression of ALK and, therefore, NeuroD1 appears to act mainly through ALK to promote the proliferation of neuroblastoma cells. Furthermore, we showed that NeuroD1 directly bound to the promoter region of ALK gene. In addition, the particular E‐box in the promoter was responsible for NeuroD1‐mediated ALK expression. These results indicate that ALK should be a direct target gene of NeuroD1. Finally, the expressions of NeuroD1 and ALK in the early tumor lesions of neuroblastoma model mice coincided in vivo. We conclude that the novel mechanism would regulate the expression of ALK in neuroblastoma and that NeuroD1 should be significantly involved in neuroblastoma tumorigenesis.
In previous report, we showed that NeuroD1 regulated migration of neuroblastoma cells. Here, we found another function that NeuroD1 also promotes the proliferation of both human neuroblastoma cell lines and tumor‐initiating cells from model mice by inducing ALK expression. |
doi_str_mv | 10.1111/cas.12628 |
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In previous report, we showed that NeuroD1 regulated migration of neuroblastoma cells. Here, we found another function that NeuroD1 also promotes the proliferation of both human neuroblastoma cell lines and tumor‐initiating cells from model mice by inducing ALK expression.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.12628</identifier><identifier>PMID: 25652313</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>ALK ; ALK protein ; Animals ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - physiology ; Beta2 protein ; Cancer ; Cell culture ; Cell growth ; Cell proliferation ; Cell Proliferation - genetics ; Cell Transformation, Neoplastic - genetics ; Deoxyribonucleic acid ; DNA ; DNA-Binding Proteins - genetics ; Genes ; Humans ; Intercellular Signaling Peptides and Proteins - biosynthesis ; Intercellular Signaling Peptides and Proteins - genetics ; Medical prognosis ; Mice ; Motility ; N-Myc Proto-Oncogene Protein ; Nerve Tissue Proteins - biosynthesis ; Nerve Tissue Proteins - genetics ; Neural crest ; Neuroblastoma ; Neuroblastoma - genetics ; Neuroblastoma - pathology ; Neuroblastoma cells ; NeuroD1 ; Original ; Pediatrics ; Phenotypes ; Plasmids ; proliferation ; Promoter Regions, Genetic - genetics ; Proto-Oncogene Proteins - genetics ; R&D ; Receptor Protein-Tyrosine Kinases - biosynthesis ; Receptor Protein-Tyrosine Kinases - metabolism ; Research & development ; RNA Interference ; RNA, Small Interfering ; Solid tumors ; Spheroids, Cellular - cytology ; Transcription factors ; Tumor Cells, Cultured ; Tumorigenesis ; Tumors ; tumorsphere</subject><ispartof>Cancer science, 2015-04, Vol.106 (4), p.390-396</ispartof><rights>2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.</rights><rights>2015. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5668-e048bf5b80095bd47783248cb81b81cc6f47d32c2a74a94eef7eba69c476135c3</citedby><cites>FETCH-LOGICAL-c5668-e048bf5b80095bd47783248cb81b81cc6f47d32c2a74a94eef7eba69c476135c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409882/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409882/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25652313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Fangjin</creatorcontrib><creatorcontrib>Kishida, Satoshi</creatorcontrib><creatorcontrib>Mu, Ping</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><creatorcontrib>Cao, Dongliang</creatorcontrib><creatorcontrib>Tsubota, Shoma</creatorcontrib><creatorcontrib>Kadomatsu, Kenji</creatorcontrib><title>NeuroD1 promotes neuroblastoma cell growth by inducing the expression of ALK</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Neuroblastoma is derived from the sympathetic neuronal lineage of neural crest cells, and is the most frequently observed of the extracranial pediatric solid tumors. The neuronal differentiation factor, NeuroD1, has previously been shown to promote cell motility in neuroblastoma by suppressing the expression of Slit2. Here we report that NeuroD1 is also involved in the proliferation of neuroblastoma cells, including human cell lines and primary tumorspheres cultured from the tumor tissues of model mice. Interestingly, the growth inhibition of neuroblastoma cells induced by knockdown of NeuroD1 was accompanied by a reduction of ALK expression. ALK is known to be one of the important predisposition genes for neuroblastoma. The phenotype resulting from knockdown of NeuroD1 was suppressed by forced expression of ALK and, therefore, NeuroD1 appears to act mainly through ALK to promote the proliferation of neuroblastoma cells. Furthermore, we showed that NeuroD1 directly bound to the promoter region of ALK gene. In addition, the particular E‐box in the promoter was responsible for NeuroD1‐mediated ALK expression. These results indicate that ALK should be a direct target gene of NeuroD1. Finally, the expressions of NeuroD1 and ALK in the early tumor lesions of neuroblastoma model mice coincided in vivo. We conclude that the novel mechanism would regulate the expression of ALK in neuroblastoma and that NeuroD1 should be significantly involved in neuroblastoma tumorigenesis.
In previous report, we showed that NeuroD1 regulated migration of neuroblastoma cells. Here, we found another function that NeuroD1 also promotes the proliferation of both human neuroblastoma cell lines and tumor‐initiating cells from model mice by inducing ALK expression.</description><subject>ALK</subject><subject>ALK protein</subject><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - physiology</subject><subject>Beta2 protein</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Genes</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - biosynthesis</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>Motility</subject><subject>N-Myc Proto-Oncogene Protein</subject><subject>Nerve Tissue Proteins - biosynthesis</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Neural crest</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - genetics</subject><subject>Neuroblastoma - pathology</subject><subject>Neuroblastoma cells</subject><subject>NeuroD1</subject><subject>Original</subject><subject>Pediatrics</subject><subject>Phenotypes</subject><subject>Plasmids</subject><subject>proliferation</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>R&D</subject><subject>Receptor Protein-Tyrosine Kinases - biosynthesis</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Research & development</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Solid tumors</subject><subject>Spheroids, Cellular - cytology</subject><subject>Transcription factors</subject><subject>Tumor Cells, Cultured</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>tumorsphere</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkV1LHDEUhoNU1KoX_oES6I29GM3X5OOmsGztBy56YXsdMtkzuyMzk20yU91_36xrRQVpSEhIHh7OyYvQCSVnNI9z79IZZZLpHXRAuTCFIkS-ezirwhDO9tH7lG4J4VIYsYf2WSlLxik_QLMrGGP4QvEqhi4MkHC_uahal4bQOeyhbfEihrthias1bvr56Jt-gYclYLhfRUipCT0ONZ7MLo_Qbu3aBMeP-yH69fXi5_R7Mbv-9mM6mRW-lFIXQISu6rLShJiymgulNGdC-0rTPL2XtVBzzjxzSjgjAGoFlZPGCyUpLz0_RJ-33tVYdTD30A_RtXYVm87FtQ2usS9f-mZpF-GPFYIYrVkWnD4KYvg9Qhps16RNq66HMCZLc0GsZIbQ_6NSlXkZYTL68RV6G8bY55-wjGmjmNFKZOrTlvIxpBShfqqbEruJ0-Y47UOcmf3wvNEn8l9-GTjfAndNC-u3TXY6udkq_wLs5Kj5</recordid><startdate>201504</startdate><enddate>201504</enddate><creator>Lu, Fangjin</creator><creator>Kishida, Satoshi</creator><creator>Mu, Ping</creator><creator>Huang, Peng</creator><creator>Cao, Dongliang</creator><creator>Tsubota, Shoma</creator><creator>Kadomatsu, Kenji</creator><general>John Wiley & Sons, Inc</general><general>BlackWell Publishing Ltd</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>201504</creationdate><title>NeuroD1 promotes neuroblastoma cell growth by inducing the expression of ALK</title><author>Lu, Fangjin ; Kishida, Satoshi ; Mu, Ping ; Huang, Peng ; Cao, Dongliang ; Tsubota, Shoma ; Kadomatsu, Kenji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5668-e048bf5b80095bd47783248cb81b81cc6f47d32c2a74a94eef7eba69c476135c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>ALK</topic><topic>ALK protein</topic><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - physiology</topic><topic>Beta2 protein</topic><topic>Cancer</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Genes</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - biosynthesis</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Medical prognosis</topic><topic>Mice</topic><topic>Motility</topic><topic>N-Myc Proto-Oncogene Protein</topic><topic>Nerve Tissue Proteins - biosynthesis</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Neural crest</topic><topic>Neuroblastoma</topic><topic>Neuroblastoma - genetics</topic><topic>Neuroblastoma - pathology</topic><topic>Neuroblastoma cells</topic><topic>NeuroD1</topic><topic>Original</topic><topic>Pediatrics</topic><topic>Phenotypes</topic><topic>Plasmids</topic><topic>proliferation</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>R&D</topic><topic>Receptor Protein-Tyrosine Kinases - biosynthesis</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Research & development</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Solid tumors</topic><topic>Spheroids, Cellular - cytology</topic><topic>Transcription factors</topic><topic>Tumor Cells, Cultured</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>tumorsphere</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Fangjin</creatorcontrib><creatorcontrib>Kishida, Satoshi</creatorcontrib><creatorcontrib>Mu, Ping</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><creatorcontrib>Cao, Dongliang</creatorcontrib><creatorcontrib>Tsubota, Shoma</creatorcontrib><creatorcontrib>Kadomatsu, Kenji</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest Biological Science Journals</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Fangjin</au><au>Kishida, Satoshi</au><au>Mu, Ping</au><au>Huang, Peng</au><au>Cao, Dongliang</au><au>Tsubota, Shoma</au><au>Kadomatsu, Kenji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NeuroD1 promotes neuroblastoma cell growth by inducing the expression of ALK</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2015-04</date><risdate>2015</risdate><volume>106</volume><issue>4</issue><spage>390</spage><epage>396</epage><pages>390-396</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Neuroblastoma is derived from the sympathetic neuronal lineage of neural crest cells, and is the most frequently observed of the extracranial pediatric solid tumors. The neuronal differentiation factor, NeuroD1, has previously been shown to promote cell motility in neuroblastoma by suppressing the expression of Slit2. Here we report that NeuroD1 is also involved in the proliferation of neuroblastoma cells, including human cell lines and primary tumorspheres cultured from the tumor tissues of model mice. Interestingly, the growth inhibition of neuroblastoma cells induced by knockdown of NeuroD1 was accompanied by a reduction of ALK expression. ALK is known to be one of the important predisposition genes for neuroblastoma. The phenotype resulting from knockdown of NeuroD1 was suppressed by forced expression of ALK and, therefore, NeuroD1 appears to act mainly through ALK to promote the proliferation of neuroblastoma cells. Furthermore, we showed that NeuroD1 directly bound to the promoter region of ALK gene. In addition, the particular E‐box in the promoter was responsible for NeuroD1‐mediated ALK expression. These results indicate that ALK should be a direct target gene of NeuroD1. Finally, the expressions of NeuroD1 and ALK in the early tumor lesions of neuroblastoma model mice coincided in vivo. We conclude that the novel mechanism would regulate the expression of ALK in neuroblastoma and that NeuroD1 should be significantly involved in neuroblastoma tumorigenesis.
In previous report, we showed that NeuroD1 regulated migration of neuroblastoma cells. Here, we found another function that NeuroD1 also promotes the proliferation of both human neuroblastoma cell lines and tumor‐initiating cells from model mice by inducing ALK expression.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>25652313</pmid><doi>10.1111/cas.12628</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | ALK ALK protein Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - physiology Beta2 protein Cancer Cell culture Cell growth Cell proliferation Cell Proliferation - genetics Cell Transformation, Neoplastic - genetics Deoxyribonucleic acid DNA DNA-Binding Proteins - genetics Genes Humans Intercellular Signaling Peptides and Proteins - biosynthesis Intercellular Signaling Peptides and Proteins - genetics Medical prognosis Mice Motility N-Myc Proto-Oncogene Protein Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - genetics Neural crest Neuroblastoma Neuroblastoma - genetics Neuroblastoma - pathology Neuroblastoma cells NeuroD1 Original Pediatrics Phenotypes Plasmids proliferation Promoter Regions, Genetic - genetics Proto-Oncogene Proteins - genetics R&D Receptor Protein-Tyrosine Kinases - biosynthesis Receptor Protein-Tyrosine Kinases - metabolism Research & development RNA Interference RNA, Small Interfering Solid tumors Spheroids, Cellular - cytology Transcription factors Tumor Cells, Cultured Tumorigenesis Tumors tumorsphere |
title | NeuroD1 promotes neuroblastoma cell growth by inducing the expression of ALK |
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