FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2891391803> ?p ?o ?g. }

• W2891391803 endingPage "17165" @default.
• W2891391803 startingPage "17154" @default.
• W2891391803 abstract "Long noncoding RNAs (lncRNAs) are vital players in cancers, including hepatocellular carcinoma (HCC). We previously identified an lncRNA, GAS8-AS1, that is located in intron 2 of GAS8. However, its involvement in HCC is still largely unknown. In this study, we report that both GAS8-AS1 and its host gene GAS8 act as HCC tumor suppressors. We found that expression of GAS8-AS1 or GAS8 is significantly decreased in HCC tissues and is associated with a poor prognosis among HCC patients. Interestingly, lncRNA GAS8-AS1 could promote GAS8 transcription. We detected a CpG island in the GAS8 promoter, but lncRNA GAS8-AS1 did not affect DNA methylation at this GAS8 promoter site. Moreover, we identified two GAS8-AS1–interacting proteins, mixed-lineage leukemia 1 (MLL1), a histone 3 Lys-4 (H3K4) methyltransferase, and its partner WD-40 repeat protein 5 (WDR5). RNA pulldown, ChIP, and RNA immunoprecipitation assays revealed that GAS8-AS1 is required for maintaining the GAS8 promoter in an open chromatin state by recruiting the MLL1/WDR5 complex and for enhancing RNA polymerase II activity and GAS8 transcription. Of note, GAS8-AS1–dependent GAS8 hyperactivation inhibited malignant transformation of hepatocytes. Our results provide important insights into how lncRNA GAS8-AS1 suppresses HCC development and suggest potential strategies for treating patients with liver cancer. Long noncoding RNAs (lncRNAs) are vital players in cancers, including hepatocellular carcinoma (HCC). We previously identified an lncRNA, GAS8-AS1, that is located in intron 2 of GAS8. However, its involvement in HCC is still largely unknown. In this study, we report that both GAS8-AS1 and its host gene GAS8 act as HCC tumor suppressors. We found that expression of GAS8-AS1 or GAS8 is significantly decreased in HCC tissues and is associated with a poor prognosis among HCC patients. Interestingly, lncRNA GAS8-AS1 could promote GAS8 transcription. We detected a CpG island in the GAS8 promoter, but lncRNA GAS8-AS1 did not affect DNA methylation at this GAS8 promoter site. Moreover, we identified two GAS8-AS1–interacting proteins, mixed-lineage leukemia 1 (MLL1), a histone 3 Lys-4 (H3K4) methyltransferase, and its partner WD-40 repeat protein 5 (WDR5). RNA pulldown, ChIP, and RNA immunoprecipitation assays revealed that GAS8-AS1 is required for maintaining the GAS8 promoter in an open chromatin state by recruiting the MLL1/WDR5 complex and for enhancing RNA polymerase II activity and GAS8 transcription. Of note, GAS8-AS1–dependent GAS8 hyperactivation inhibited malignant transformation of hepatocytes. Our results provide important insights into how lncRNA GAS8-AS1 suppresses HCC development and suggest potential strategies for treating patients with liver cancer." @default.
• W2891391803 created "2018-09-27" @default.
• W2891391803 creator A5003302088 @default.
• W2891391803 creator A5023363049 @default.
• W2891391803 creator A5036497246 @default.
• W2891391803 creator A5062225206 @default.
• W2891391803 creator A5067171110 @default.
• W2891391803 creator A5070151668 @default.
• W2891391803 creator A5081222889 @default.
• W2891391803 date "2018-11-01" @default.
• W2891391803 modified "2023-10-18" @default.
• W2891391803 title "The long noncoding RNA GAS8-AS1 suppresses hepatocarcinogenesis by epigenetically activating the tumor suppressor GAS8" @default.
• W2891391803 cites W1487500629 @default.
• W2891391803 cites W1500465327 @default.
• W2891391803 cites W1981989535 @default.
• W2891391803 cites W1992662525 @default.
• W2891391803 cites W1999746344 @default.
• W2891391803 cites W2001728145 @default.
• W2891391803 cites W2005148604 @default.
• W2891391803 cites W2008041603 @default.
• W2891391803 cites W2018005623 @default.
• W2891391803 cites W2025150647 @default.
• W2891391803 cites W2032183472 @default.
• W2891391803 cites W2038926092 @default.
• W2891391803 cites W2049868369 @default.
• W2891391803 cites W2070777085 @default.
• W2891391803 cites W2071271349 @default.
• W2891391803 cites W2087377443 @default.
• W2891391803 cites W2092467693 @default.
• W2891391803 cites W2094338705 @default.
• W2891391803 cites W2096858457 @default.
• W2891391803 cites W2097808331 @default.
• W2891391803 cites W2099984271 @default.
• W2891391803 cites W2117633931 @default.
• W2891391803 cites W2137052325 @default.
• W2891391803 cites W2144137532 @default.
• W2891391803 cites W2146573461 @default.
• W2891391803 cites W2148958327 @default.
• W2891391803 cites W2153268494 @default.
• W2891391803 cites W2165154206 @default.
• W2891391803 cites W2289297923 @default.
• W2891391803 cites W2343311949 @default.
• W2891391803 cites W2495497541 @default.
• W2891391803 cites W2498082946 @default.
• W2891391803 cites W2510509415 @default.
• W2891391803 cites W2606700140 @default.
• W2891391803 cites W2625600561 @default.
• W2891391803 cites W2735687500 @default.
• W2891391803 cites W2751404335 @default.
• W2891391803 doi "https://doi.org/10.1074/jbc.ra118.003055" @default.
• W2891391803 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6222094" @default.
• W2891391803 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30228180" @default.
• W2891391803 hasPublicationYear "2018" @default.
• W2891391803 type Work @default.
• W2891391803 sameAs 2891391803 @default.
• W2891391803 citedByCount "40" @default.
• W2891391803 countsByYear W28913918032019 @default.
• W2891391803 countsByYear W28913918032020 @default.
• W2891391803 countsByYear W28913918032021 @default.
• W2891391803 countsByYear W28913918032022 @default.
• W2891391803 countsByYear W28913918032023 @default.
• W2891391803 crossrefType "journal-article" @default.
• W2891391803 hasAuthorship W2891391803A5003302088 @default.
• W2891391803 hasAuthorship W2891391803A5023363049 @default.
• W2891391803 hasAuthorship W2891391803A5036497246 @default.
• W2891391803 hasAuthorship W2891391803A5062225206 @default.
• W2891391803 hasAuthorship W2891391803A5067171110 @default.
• W2891391803 hasAuthorship W2891391803A5070151668 @default.
• W2891391803 hasAuthorship W2891391803A5081222889 @default.
• W2891391803 hasBestOaLocation W28913918031 @default.
• W2891391803 hasConcept C101762097 @default.
• W2891391803 hasConcept C104317684 @default.
• W2891391803 hasConcept C134320426 @default.
• W2891391803 hasConcept C138885662 @default.
• W2891391803 hasConcept C150194340 @default.
• W2891391803 hasConcept C153911025 @default.
• W2891391803 hasConcept C179926584 @default.
• W2891391803 hasConcept C190727270 @default.
• W2891391803 hasConcept C33288867 @default.
• W2891391803 hasConcept C41895202 @default.
• W2891391803 hasConcept C502942594 @default.
• W2891391803 hasConcept C54355233 @default.
• W2891391803 hasConcept C62203573 @default.
• W2891391803 hasConcept C64350747 @default.
• W2891391803 hasConcept C67705224 @default.
• W2891391803 hasConcept C83640560 @default.
• W2891391803 hasConcept C86803240 @default.
• W2891391803 hasConcept C91965660 @default.
• W2891391803 hasConcept C94671646 @default.
• W2891391803 hasConceptScore W2891391803C101762097 @default.
• W2891391803 hasConceptScore W2891391803C104317684 @default.
• W2891391803 hasConceptScore W2891391803C134320426 @default.
• W2891391803 hasConceptScore W2891391803C138885662 @default.
• W2891391803 hasConceptScore W2891391803C150194340 @default.
• W2891391803 hasConceptScore W2891391803C153911025 @default.
• W2891391803 hasConceptScore W2891391803C179926584 @default.
• W2891391803 hasConceptScore W2891391803C190727270 @default.
• W2891391803 hasConceptScore W2891391803C33288867 @default.

• next