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Down-regulation of SYK by promoter CpG island hypermethylation and its potential role in hepatocellular carcinoma : 간암에서 SYK의 프로모터 CpG island 과메틸화에 의한 발현소실 및 종양억제자로서의 역할에 대한 연구
DC Field | Value | Language |
---|---|---|
dc.contributor.advisor | 강경훈 | - |
dc.contributor.author | 신소현 | - |
dc.date.accessioned | 2017-07-14T01:14:53Z | - |
dc.date.available | 2017-07-14T01:14:53Z | - |
dc.date.issued | 2014-02 | - |
dc.identifier.other | 000000016643 | - |
dc.identifier.uri | https://hdl.handle.net/10371/121763 | - |
dc.description | 학위논문 (박사)-- 서울대학교 대학원 : 협동과정 종양생물학전공, 2014. 2. 강경훈. | - |
dc.description.abstract | The spleen tyrosine kinase (SYK) has predominantly been studied in hematopoietic cells in which it is involved in immunoreceptor-mediated signaling. However, SYK expression is evidenced in numerous nonhematopoietic cells and its down-regulation has been shown to be involved in tumor formation and progression. Our team has reported that SYK promoter methylation identifies a subset of hepatocellular carcinoma (HCC) with poor prognosis but little is known regarding a biological role of SYK in HCC. We found that SYK promoter methylation is a common event in HCC and is closely associated with its expression. We established stable HCC cell lines that contain SYK gene in inducible expression vector and then compared RNA expression profiles of HCC cell lines with or without induction of SYK. Gene ontology analysis revealed that the SYK-regulated genes are enriched among genes involved in cell adhesion and cell growth. Indeed, we found that SYK increased cell adhesion to fibronectin and decreased cell proliferation. Induced expression of SYK decreased cell migration and invasion by coordination with adhesion molecules as well as suppression of Rho-family GTPases. Our findings suggest that SYK loss is implicated in cell proliferation, migration, and invasion of HCC cells. | - |
dc.description.tableofcontents | Abstract
Contents List of Tables List of Figures Introduction Material and Methods Cell lines and 5-Aza-dC treatment Tet-on inducible expression system GFP tagged SYK expression vector and transfection Expression microarray Sodium bisulfite modification and methylation analysis RT-PCR Western blot Colony formation assay Cell proliferation assay Cell migration and invasion assay Immunofluorescence Cell adhesion assay Coimmunoprecipitation Statistical Analysis Results Correlation of SYK expression with methylation status Gene expression profiling Gene ontology analysis of SYK-dependent genes in HCC cells Expression of SYK suppresses cell growth Effect of SYK on cell adhesion, migration and invasion Cellular redistribution of SYK following adhesion to fibronectin SYK associates with cytoskeleton and adhesion molecules Expression of SYK cause a suppression of Rho-Family GTPases and stress fiber formation Discussion References Abstract in Korean | - |
dc.format | application/pdf | - |
dc.format.extent | 3673462 bytes | - |
dc.format.medium | application/pdf | - |
dc.language.iso | en | - |
dc.publisher | 서울대학교 대학원 | - |
dc.subject.ddc | 616 | - |
dc.title | Down-regulation of SYK by promoter CpG island hypermethylation and its potential role in hepatocellular carcinoma | - |
dc.title.alternative | 간암에서 SYK의 프로모터 CpG island 과메틸화에 의한 발현소실 및 종양억제자로서의 역할에 대한 연구 | - |
dc.type | Thesis | - |
dc.contributor.AlternativeAuthor | Shin So-Hyun | - |
dc.description.degree | Doctor | - |
dc.citation.pages | 71 | - |
dc.contributor.affiliation | 의과대학 협동과정 종양생물학전공 | - |
dc.date.awarded | 2014-02 | - |
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