FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2005366231> ?p ?o ?g. }

• W2005366231 abstract "Abstract Background MYCT1, previously named MTLC, is a novel candidate tumor suppressor gene. MYCT1 was cloned from laryngeal squamous cell cancer (LSCC) and has been found to be down-regulated in LSCC; however, the regulatory details have not been fully elucidated. Methods Here, we sought to investigate the methylation status of the CpG islands of MYCT1 and mRNA levels by bisulfite-specific PCR (BSP) based on sequencing restriction enzyme digestion, reverse transcription and real-time quantitative polymerase chain reaction (RQ-PCR). The function of specific sites in the proximal promoter of MYCT1 in LSCC was measured by transient transfection, luciferase assays, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation assay (ChIP). Results The results suggested hypermethylation of 12 CpG sites of the promoter in both laryngeal cancer tissues and the laryngeal cancer line Hep-2 cell. The hypermethylation of the site CGCG (−695 to −692), which has been identified as the c-Myc binding site, was identified in laryngeal cancer tissues (59/73) compared to paired mucosa (13/73); in addition, statistical analysis revealed that the methylation status of this site significantly correlated with cancer cell differentiation(p < 0.01). The mRNA level of MYCT1 increased in Hep-2 cells treated with 5-aza-C (p < 0.01). The luciferase activity from mutant transfectants pGL3 -MYCT1m (−852/+12, mut-695-C > A, mut-693-C > G) was significantly reduced compared with the wild type pGL3- MYCT1 (−852/+12), while the luciferase activity from wild transfectants pGL3 -MYCT1 (−852/+12) rose after 5-aza treatment in Hep-2 cells. Finally, EMSA and ChIP confirmed that the methylation of the CGCG (−695 to −692) site prevented c-Myc from binding of the site and demethylation treatment of the 5′ flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p < 0.01). Conclusion In summary, this study concluded that hypermethylation contributed to the transcriptional down-regulation of MYCT1 and could inhibit cancer cell differentiation in LSCC. DNA methylation of the CGCG site (−695 to −692) of MYCT1 altered the promoter activity by interfering with its binding to c-Myc in LSCC. Epigenetic therapy of reactivating MYCT1 by 5-aza should be further evaluated in clinical trails of LSCC." @default.
• W2005366231 created "2016-06-24" @default.
• W2005366231 creator A5017085439 @default.
• W2005366231 creator A5025095484 @default.
• W2005366231 creator A5035071933 @default.
• W2005366231 creator A5052099130 @default.
• W2005366231 creator A5056742068 @default.
• W2005366231 creator A5075982592 @default.
• W2005366231 creator A5090654075 @default.
• W2005366231 date "2012-06-06" @default.
• W2005366231 modified "2023-10-13" @default.
• W2005366231 title "Promoter hypermethylation-induced transcriptional down-regulation of the gene MYCT1in laryngeal squamous cell carcinoma" @default.
• W2005366231 cites W151228450 @default.
• W2005366231 cites W1935082899 @default.
• W2005366231 cites W1970410800 @default.
• W2005366231 cites W1981296878 @default.
• W2005366231 cites W1984879354 @default.
• W2005366231 cites W1986449954 @default.
• W2005366231 cites W1998450146 @default.
• W2005366231 cites W2007811208 @default.
• W2005366231 cites W2014313104 @default.
• W2005366231 cites W2027322859 @default.
• W2005366231 cites W2034502545 @default.
• W2005366231 cites W2036881307 @default.
• W2005366231 cites W2037660359 @default.
• W2005366231 cites W2040848192 @default.
• W2005366231 cites W2044296075 @default.
• W2005366231 cites W2055641636 @default.
• W2005366231 cites W2062348957 @default.
• W2005366231 cites W2069746308 @default.
• W2005366231 cites W2070152513 @default.
• W2005366231 cites W2079458256 @default.
• W2005366231 cites W2084431624 @default.
• W2005366231 cites W2086274096 @default.
• W2005366231 cites W2087832022 @default.
• W2005366231 cites W2088416146 @default.
• W2005366231 cites W2089601677 @default.
• W2005366231 cites W2094777003 @default.
• W2005366231 cites W2098825279 @default.
• W2005366231 cites W2116090660 @default.
• W2005366231 cites W2126150981 @default.
• W2005366231 cites W2127711905 @default.
• W2005366231 cites W2131577336 @default.
• W2005366231 cites W2132593080 @default.
• W2005366231 cites W2135515956 @default.
• W2005366231 cites W2136743442 @default.
• W2005366231 cites W2158035460 @default.
• W2005366231 cites W4236512674 @default.
• W2005366231 doi "https://doi.org/10.1186/1471-2407-12-219" @default.
• W2005366231 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3472177" @default.
• W2005366231 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22672838" @default.
• W2005366231 hasPublicationYear "2012" @default.
• W2005366231 type Work @default.
• W2005366231 sameAs 2005366231 @default.
• W2005366231 citedByCount "20" @default.
• W2005366231 countsByYear W20053662312013 @default.
• W2005366231 countsByYear W20053662312014 @default.
• W2005366231 countsByYear W20053662312015 @default.
• W2005366231 countsByYear W20053662312016 @default.
• W2005366231 countsByYear W20053662312017 @default.
• W2005366231 countsByYear W20053662312018 @default.
• W2005366231 countsByYear W20053662312019 @default.
• W2005366231 countsByYear W20053662312020 @default.
• W2005366231 countsByYear W20053662312021 @default.
• W2005366231 countsByYear W20053662312022 @default.
• W2005366231 countsByYear W20053662312023 @default.
• W2005366231 crossrefType "journal-article" @default.
• W2005366231 hasAuthorship W2005366231A5017085439 @default.
• W2005366231 hasAuthorship W2005366231A5025095484 @default.
• W2005366231 hasAuthorship W2005366231A5035071933 @default.
• W2005366231 hasAuthorship W2005366231A5052099130 @default.
• W2005366231 hasAuthorship W2005366231A5056742068 @default.
• W2005366231 hasAuthorship W2005366231A5075982592 @default.
• W2005366231 hasAuthorship W2005366231A5090654075 @default.
• W2005366231 hasBestOaLocation W20053662311 @default.
• W2005366231 hasConcept C101762097 @default.
• W2005366231 hasConcept C104317684 @default.
• W2005366231 hasConcept C111335760 @default.
• W2005366231 hasConcept C134320426 @default.
• W2005366231 hasConcept C140173407 @default.
• W2005366231 hasConcept C150194340 @default.
• W2005366231 hasConcept C153911025 @default.
• W2005366231 hasConcept C190727270 @default.
• W2005366231 hasConcept C33288867 @default.
• W2005366231 hasConcept C502942594 @default.
• W2005366231 hasConcept C54009773 @default.
• W2005366231 hasConcept C54355233 @default.
• W2005366231 hasConcept C86803240 @default.
• W2005366231 hasConceptScore W2005366231C101762097 @default.
• W2005366231 hasConceptScore W2005366231C104317684 @default.
• W2005366231 hasConceptScore W2005366231C111335760 @default.
• W2005366231 hasConceptScore W2005366231C134320426 @default.
• W2005366231 hasConceptScore W2005366231C140173407 @default.
• W2005366231 hasConceptScore W2005366231C150194340 @default.
• W2005366231 hasConceptScore W2005366231C153911025 @default.
• W2005366231 hasConceptScore W2005366231C190727270 @default.
• W2005366231 hasConceptScore W2005366231C33288867 @default.
• W2005366231 hasConceptScore W2005366231C502942594 @default.
• W2005366231 hasConceptScore W2005366231C54009773 @default.
• W2005366231 hasConceptScore W2005366231C54355233 @default.

• next