The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells.
Identifieur interne : 000052 ( PubMed/Curation ); précédent : 000051; suivant : 000053The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells.
Auteurs : Tianhong Pan [États-Unis] ; Julie Zhu ; Wen Hwu ; Joseph JankovicSource :
- PloS one ; 2012.
English descriptors
- KwdEn :
- Cell Line, Tumor, Cell Survival (radiation effects), Dopamine (metabolism), Dopamine (pharmacology), Dopaminergic Neurons (metabolism), Gene Expression (radiation effects), Humans, Melanins (biosynthesis), Melanins (genetics), Melanoma, Monophenol Monooxygenase (metabolism), Organ Specificity, Parkinson Disease, Signal Transduction (radiation effects), Skin Neoplasms, Tyrosine 3-Monooxygenase (metabolism), Ultraviolet Rays, alpha-Synuclein (genetics), alpha-Synuclein (metabolism).
- MESH :
- chemical , biosynthesis : Melanins.
- chemical , genetics : Melanins, alpha-Synuclein.
- chemical , metabolism : Dopamine, Monophenol Monooxygenase, Tyrosine 3-Monooxygenase, alpha-Synuclein.
- chemical , pharmacology : Dopamine.
- metabolism : Dopaminergic Neurons.
- radiation effects : Cell Survival, Gene Expression, Signal Transduction.
- Cell Line, Tumor, Humans, Melanoma, Organ Specificity, Parkinson Disease, Skin Neoplasms, Ultraviolet Rays.
Abstract
The relatively high co-occurrence of Parkinson's disease (PD) and melanoma has been established by a large number of epidemiological studies. However, a clear biological explanation for this finding is still lacking. Ultra-violet radiation (UVR)-induced skin melanin synthesis is a defense mechanism against UVR-induced damage relevant to the initiation of melanoma, whereas, increased neuromelanin (NM), the melanin synthesized in dopaminergic neurons, may enhance the susceptibility to oxidative stress-induced neuronal injury relevant to PD. SNCA is a PD-causing gene coding for alpha-Synuclein (α-Syn) that expresses not only in brain, but also in skin as well as in tumors, such as melanoma. The findings that α-Syn can interact with tyrosinase (TYR) and inhibit tyrosine hydroxylase (TH), both of which are enzymes involved in the biosynthesis of melanin and dopamine (DA), led us to propose that α-Syn may participate in the regulation of melanin synthesis. In this study, by applying ultraviolet B (UVB) light, a physiologically relevant stimulus of melanogenesis, we detected melanin synthesis in A375 and SK-MEL-28 melanoma cells and in SH-SY5Y and PC12 dopaminergic neuronal cells and determined effects of α-Syn on melanin synthesis. Our results showed that UVB light exposure increased melanin synthesis in all 4 cell lines. However, we found that α-Syn expression reduced UVB light-induced increase of melanin synthesis and that melanin content was lower when melanoma cells were expressed with α-Syn, indicating that α-Syn may have inhibitory effects on melanin synthesis in melanoma cells. Different from melanoma cells, the melanin content was higher in α-Syn-over-expressed dopaminergic neuronal SH-SY5Y and PC12 cells, cellular models of PD, than that in non-α-Syn-expressed control cells. We concluded that α-Syn could be one of the points responsible for the positive association between PD and melanoma via its differential roles in melanin synthesis in melanoma cells and in dopaminergic neuronal cells.
DOI: 10.1371/journal.pone.0045183
PubMed: 23028833
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells.</title><author><name sortKey="Pan, Tianhong" sort="Pan, Tianhong" uniqKey="Pan T" first="Tianhong" last="Pan">Tianhong Pan</name><affiliation wicri:level="1"><nlm:affiliation>Neurology Department, Parkinson Disease Research Laboratory, Baylor College of Medicine, Houston, Texas, USA. tpan@bcm.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neurology Department, Parkinson Disease Research Laboratory, Baylor College of Medicine, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Zhu, Julie" sort="Zhu, Julie" uniqKey="Zhu J" first="Julie" last="Zhu">Julie Zhu</name></author><author><name sortKey="Hwu, Wen Jen" sort="Hwu, Wen Jen" uniqKey="Hwu W" first="Wen" last="Hwu">Wen Hwu</name></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="doi">10.1371/journal.pone.0045183</idno><idno type="RBID">pubmed:23028833</idno><idno type="pmid">23028833</idno><idno type="wicri:Area/PubMed/Corpus">000052</idno><idno type="wicri:Area/PubMed/Curation">000052</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells.</title><author><name sortKey="Pan, Tianhong" sort="Pan, Tianhong" uniqKey="Pan T" first="Tianhong" last="Pan">Tianhong Pan</name><affiliation wicri:level="1"><nlm:affiliation>Neurology Department, Parkinson Disease Research Laboratory, Baylor College of Medicine, Houston, Texas, USA. tpan@bcm.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neurology Department, Parkinson Disease Research Laboratory, Baylor College of Medicine, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Zhu, Julie" sort="Zhu, Julie" uniqKey="Zhu J" first="Julie" last="Zhu">Julie Zhu</name></author><author><name sortKey="Hwu, Wen Jen" sort="Hwu, Wen Jen" uniqKey="Hwu W" first="Wen" last="Hwu">Wen Hwu</name></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name></author></analytic><series><title level="j">PloS one</title><idno type="e-ISSN">1932-6203</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line, Tumor</term><term>Cell Survival (radiation effects)</term><term>Dopamine (metabolism)</term><term>Dopamine (pharmacology)</term><term>Dopaminergic Neurons (metabolism)</term><term>Gene Expression (radiation effects)</term><term>Humans</term><term>Melanins (biosynthesis)</term><term>Melanins (genetics)</term><term>Melanoma</term><term>Monophenol Monooxygenase (metabolism)</term><term>Organ Specificity</term><term>Parkinson Disease</term><term>Signal Transduction (radiation effects)</term><term>Skin Neoplasms</term><term>Tyrosine 3-Monooxygenase (metabolism)</term><term>Ultraviolet Rays</term><term>alpha-Synuclein (genetics)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Melanins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Melanins</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Monophenol Monooxygenase</term><term>Tyrosine 3-Monooxygenase</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Cell Survival</term><term>Gene Expression</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term><term>Melanoma</term><term>Organ Specificity</term><term>Parkinson Disease</term><term>Skin Neoplasms</term><term>Ultraviolet Rays</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The relatively high co-occurrence of Parkinson's disease (PD) and melanoma has been established by a large number of epidemiological studies. However, a clear biological explanation for this finding is still lacking. Ultra-violet radiation (UVR)-induced skin melanin synthesis is a defense mechanism against UVR-induced damage relevant to the initiation of melanoma, whereas, increased neuromelanin (NM), the melanin synthesized in dopaminergic neurons, may enhance the susceptibility to oxidative stress-induced neuronal injury relevant to PD. SNCA is a PD-causing gene coding for alpha-Synuclein (α-Syn) that expresses not only in brain, but also in skin as well as in tumors, such as melanoma. The findings that α-Syn can interact with tyrosinase (TYR) and inhibit tyrosine hydroxylase (TH), both of which are enzymes involved in the biosynthesis of melanin and dopamine (DA), led us to propose that α-Syn may participate in the regulation of melanin synthesis. In this study, by applying ultraviolet B (UVB) light, a physiologically relevant stimulus of melanogenesis, we detected melanin synthesis in A375 and SK-MEL-28 melanoma cells and in SH-SY5Y and PC12 dopaminergic neuronal cells and determined effects of α-Syn on melanin synthesis. Our results showed that UVB light exposure increased melanin synthesis in all 4 cell lines. However, we found that α-Syn expression reduced UVB light-induced increase of melanin synthesis and that melanin content was lower when melanoma cells were expressed with α-Syn, indicating that α-Syn may have inhibitory effects on melanin synthesis in melanoma cells. Different from melanoma cells, the melanin content was higher in α-Syn-over-expressed dopaminergic neuronal SH-SY5Y and PC12 cells, cellular models of PD, than that in non-α-Syn-expressed control cells. We concluded that α-Syn could be one of the points responsible for the positive association between PD and melanoma via its differential roles in melanin synthesis in melanoma cells and in dopaminergic neuronal cells.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23028833</PMID><DateCreated><Year>2012</Year><Month>10</Month><Day>02</Day></DateCreated><DateCompleted><Year>2013</Year><Month>02</Month><Day>28</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>9</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells.</ArticleTitle><Pagination><MedlinePgn>e45183</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0045183</ELocationID><Abstract><AbstractText>The relatively high co-occurrence of Parkinson's disease (PD) and melanoma has been established by a large number of epidemiological studies. However, a clear biological explanation for this finding is still lacking. Ultra-violet radiation (UVR)-induced skin melanin synthesis is a defense mechanism against UVR-induced damage relevant to the initiation of melanoma, whereas, increased neuromelanin (NM), the melanin synthesized in dopaminergic neurons, may enhance the susceptibility to oxidative stress-induced neuronal injury relevant to PD. SNCA is a PD-causing gene coding for alpha-Synuclein (α-Syn) that expresses not only in brain, but also in skin as well as in tumors, such as melanoma. The findings that α-Syn can interact with tyrosinase (TYR) and inhibit tyrosine hydroxylase (TH), both of which are enzymes involved in the biosynthesis of melanin and dopamine (DA), led us to propose that α-Syn may participate in the regulation of melanin synthesis. In this study, by applying ultraviolet B (UVB) light, a physiologically relevant stimulus of melanogenesis, we detected melanin synthesis in A375 and SK-MEL-28 melanoma cells and in SH-SY5Y and PC12 dopaminergic neuronal cells and determined effects of α-Syn on melanin synthesis. Our results showed that UVB light exposure increased melanin synthesis in all 4 cell lines. However, we found that α-Syn expression reduced UVB light-induced increase of melanin synthesis and that melanin content was lower when melanoma cells were expressed with α-Syn, indicating that α-Syn may have inhibitory effects on melanin synthesis in melanoma cells. Different from melanoma cells, the melanin content was higher in α-Syn-over-expressed dopaminergic neuronal SH-SY5Y and PC12 cells, cellular models of PD, than that in non-α-Syn-expressed control cells. We concluded that α-Syn could be one of the points responsible for the positive association between PD and melanoma via its differential roles in melanin synthesis in melanoma cells and in dopaminergic neuronal cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Tianhong</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Neurology Department, Parkinson Disease Research Laboratory, Baylor College of Medicine, Houston, Texas, USA. tpan@bcm.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Julie</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Hwu</LastName><ForeName>Wen-Jen</ForeName><Initials>WJ</Initials></Author><Author ValidYN="Y"><LastName>Jankovic</LastName><ForeName>Joseph</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal 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UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3446957</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>6</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>8</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="epublish"><Year>2012</Year><Month>9</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>10</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>10</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>3</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1371/journal.pone.0045183</ArticleId><ArticleId 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