Matches in SemOpenAlex for { <https://semopenalex.org/work/W3150796685> ?p ?o ?g. }
- W3150796685 abstract "Abstract Gain of chromosome 1q locus is a common cytogenetic feature associated with intracranial ependymomas; however, candidate non-coding RNAs on this locus have not been identified. Recent studies have reported somatic copy number alterations for long non coding RNA (lncRNA) FAL1/FALEC residing on chromosome 1q to stabilize BMI1, an epigenetic repressor and PRC1 component, leading with to downregulation of p21/CDKN1A tumor suppressor gene. We aimed to study the role of FAL1 in ependymomas, its association with 1q gain, BMI1/p21 regulatory axis and clinicopathological parameters. Using SNP array analysis (GSE32101), 31% (discovery cohort) and 63.8% (in-house cohort) showed amplification/gain of FAL1 locus with higher prevalence in intracranial tumors. Copy number gain of FAL1 locus was significantly associated with increased FAL1 (p=0.003) and BMI1 (p=0.007) levels, and reduced p21 (p=0.001) expressions. Interestingly, gain of FAL1 locus and FAL1 transcripts did not show any association with 1q gain or RELA fusions. Subcellular localization reported FAL1 to be expressed in nuclear compartment in ependymomas. Chromatin immunoprecipitation-qPCR demonstrated in-vivo binding of BMI1 at p21 promoter locus with BMI1 target genes to be enriched in cell architecture related pathways. A 3-tier survival analysis between FAL1 gain and increased expression levels of FAL1 and BMI1 correlated with poor outcome in our cohort. Ours is the first study demonstrating gain of FAL1 locus and its interplay with the BMI1 /p21 axis in intracranial ependymomas. Further studies into this epigenetic regulatory mechanism will unravel novel driver mutations in intracranial ependymomas Highlights Somatic variations in enhancer long non-coding RNA has been recently attributed for various clinical malignancies including cancers. Gain of 1q locus is a common cytogenetic variation observed in intracranial ependymomas. Our study has demonstrated, focal amplification of enhancer lncRNA mapping to Chromosome 1q, FAL1/FALEC , to be involved in oncogenicity/ progression of ependymomas. Moreover, our data suggests a positive association with BMI1 (a PRC1 component) with FAL1 levels, indicating downregulation of BMI1 target gene involved in cell cycle, p21. Furthermore, a 3-tier prognosis analysis (between FAL1 gain, FAL1 and BMI1 expressions) suggests a negative survival outcome. Our study highlights the importance of somatic variation in non-coding genome with ependymoma survival." @default.
- W3150796685 created "2021-04-13" @default.
- W3150796685 creator A5006494004 @default.
- W3150796685 creator A5023515402 @default.
- W3150796685 creator A5031232082 @default.
- W3150796685 creator A5034670982 @default.
- W3150796685 creator A5039362893 @default.
- W3150796685 creator A5062735427 @default.
- W3150796685 creator A5064979397 @default.
- W3150796685 creator A5079762592 @default.
- W3150796685 creator A5084725442 @default.
- W3150796685 creator A5090045933 @default.
- W3150796685 date "2021-03-26" @default.
- W3150796685 modified "2023-10-16" @default.
- W3150796685 title "Focal amplification of FAL1, an oncogenic enhancer lncRNA mapping to chromosome 1q is associated with dysregulated BMI1/p21 axis and an adverse event in intracranial ependymomas" @default.
- W3150796685 cites W1526406267 @default.
- W3150796685 cites W15521340 @default.
- W3150796685 cites W1845373224 @default.
- W3150796685 cites W1937005742 @default.
- W3150796685 cites W1949037014 @default.
- W3150796685 cites W1964339879 @default.
- W3150796685 cites W1971349026 @default.
- W3150796685 cites W1974350437 @default.
- W3150796685 cites W1976133851 @default.
- W3150796685 cites W1980324442 @default.
- W3150796685 cites W1987425587 @default.
- W3150796685 cites W1993240075 @default.
- W3150796685 cites W2003870059 @default.
- W3150796685 cites W2005689681 @default.
- W3150796685 cites W2020531974 @default.
- W3150796685 cites W2027729143 @default.
- W3150796685 cites W2053430315 @default.
- W3150796685 cites W2063848388 @default.
- W3150796685 cites W2064835029 @default.
- W3150796685 cites W2067768332 @default.
- W3150796685 cites W2070262236 @default.
- W3150796685 cites W2080790343 @default.
- W3150796685 cites W2105298978 @default.
- W3150796685 cites W2105414327 @default.
- W3150796685 cites W2105507863 @default.
- W3150796685 cites W2110004488 @default.
- W3150796685 cites W2126059322 @default.
- W3150796685 cites W2128559801 @default.
- W3150796685 cites W2138753433 @default.
- W3150796685 cites W2140048538 @default.
- W3150796685 cites W2142388038 @default.
- W3150796685 cites W2145733907 @default.
- W3150796685 cites W2152338378 @default.
- W3150796685 cites W2153882021 @default.
- W3150796685 cites W2166478307 @default.
- W3150796685 cites W2171236756 @default.
- W3150796685 cites W2226760327 @default.
- W3150796685 cites W2323288618 @default.
- W3150796685 cites W2475516771 @default.
- W3150796685 cites W2509673039 @default.
- W3150796685 cites W2516200712 @default.
- W3150796685 cites W2569675702 @default.
- W3150796685 cites W2594188745 @default.
- W3150796685 cites W2714552381 @default.
- W3150796685 cites W2785109205 @default.
- W3150796685 cites W2887975472 @default.
- W3150796685 cites W2939800568 @default.
- W3150796685 cites W2968190332 @default.
- W3150796685 cites W2979774294 @default.
- W3150796685 cites W4253954633 @default.
- W3150796685 doi "https://doi.org/10.1101/2021.03.24.21254063" @default.
- W3150796685 hasPublicationYear "2021" @default.
- W3150796685 type Work @default.
- W3150796685 sameAs 3150796685 @default.
- W3150796685 citedByCount "0" @default.
- W3150796685 crossrefType "posted-content" @default.
- W3150796685 hasAuthorship W3150796685A5006494004 @default.
- W3150796685 hasAuthorship W3150796685A5023515402 @default.
- W3150796685 hasAuthorship W3150796685A5031232082 @default.
- W3150796685 hasAuthorship W3150796685A5034670982 @default.
- W3150796685 hasAuthorship W3150796685A5039362893 @default.
- W3150796685 hasAuthorship W3150796685A5062735427 @default.
- W3150796685 hasAuthorship W3150796685A5064979397 @default.
- W3150796685 hasAuthorship W3150796685A5079762592 @default.
- W3150796685 hasAuthorship W3150796685A5084725442 @default.
- W3150796685 hasAuthorship W3150796685A5090045933 @default.
- W3150796685 hasBestOaLocation W31507966851 @default.
- W3150796685 hasConcept C101762097 @default.
- W3150796685 hasConcept C104317684 @default.
- W3150796685 hasConcept C111936080 @default.
- W3150796685 hasConcept C134320426 @default.
- W3150796685 hasConcept C143589142 @default.
- W3150796685 hasConcept C150194340 @default.
- W3150796685 hasConcept C180754005 @default.
- W3150796685 hasConcept C41091548 @default.
- W3150796685 hasConcept C502942594 @default.
- W3150796685 hasConcept C54355233 @default.
- W3150796685 hasConcept C83640560 @default.
- W3150796685 hasConcept C84597430 @default.
- W3150796685 hasConcept C86803240 @default.
- W3150796685 hasConceptScore W3150796685C101762097 @default.
- W3150796685 hasConceptScore W3150796685C104317684 @default.
- W3150796685 hasConceptScore W3150796685C111936080 @default.
- W3150796685 hasConceptScore W3150796685C134320426 @default.
- W3150796685 hasConceptScore W3150796685C143589142 @default.