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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Veröffentlicht in:Cancer science 2015-04, Vol.106 (4), p.390-396
Hauptverfasser: Lu, Fangjin, Kishida, Satoshi, Mu, Ping, Huang, Peng, Cao, Dongliang, Tsubota, Shoma, Kadomatsu, Kenji
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container_issue 4
container_start_page 390
container_title Cancer science
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creator Lu, Fangjin
Kishida, Satoshi
Mu, Ping
Huang, Peng
Cao, Dongliang
Tsubota, Shoma
Kadomatsu, Kenji
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.
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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><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 &amp; 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&amp;D ; Receptor Protein-Tyrosine Kinases - biosynthesis ; Receptor Protein-Tyrosine Kinases - metabolism ; Research &amp; 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&amp;D</subject><subject>Receptor Protein-Tyrosine Kinases - biosynthesis</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Research &amp; 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 &amp; 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&amp;D</topic><topic>Receptor Protein-Tyrosine Kinases - biosynthesis</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Research &amp; 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 &amp; 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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