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SUMMARY:Signal transducing long non-coding RNAs regulating Cancer Biology 
  - professor Erwei Song from Sun Yat-sen University in China
DTSTART:20190807T113000Z
DTEND:20190807T123000Z
UID:TALK126196@talks.cam.ac.uk
CONTACT:72001
DESCRIPTION:It is becoming increasingly clear that noncoding RNAs (ncRNAs)
  may constitute a new layer of regulatory control over gene expression pro
 grams in many organisms. ncRNAs are loosely grouped into two major classes
  based on their size: small ncRNAs less than 200 nt\, and long ncRNAs (lnc
 RNAs). LncRNAs have been shown to regulate gene expression by deploying ep
 igenetic modification and modulating transcription\, mRNA splicing\, and t
 ranslation\, during which they may function as guides\, decoys\, or scaffo
 lds for gene regulating proteins. Although these models predict most of th
 e known lncRNA functions\, the detailed mechanisms are poorly elucidated. 
 In our recent study we identified a cytoplasmic lncRNA called NFκB intera
 cting long noncoding RNA (NKILA) that interacts with NFκB and represses I
 κB phosphorylation by physically hindering the phosphorylation site of I
 κB. NKILA is transcriptionally activated by NFκB signaling upon challeng
 e by proinflammatory cytokines\, and forms a negative feedback loop for NF
 κB regulation. NKILA differs from other known NFκB negative feedback loo
 ps in that it acts at the level of IκB phosphorylation\, which constitute
 s a physiological barrier to prevent NFκB over activation under condition
 s of persistently elevated IKK. As a “gate keeper” for aberrant NFκB 
 activation\, NKILA is subjected to microRNA-mediated degradation and its e
 xpression is decreased in various types of cancer including breast\, liver
 \, lung\, and colon cancers. Reduced NKILA expression in advanced cancers 
 may result in NFκB over activation and the consequential cancer metastasi
 s. Our findings have revealed a new class of lncRNAs that directly interac
 t with proteins involved in signal transduction pathways and interfere wit
 h cell signaling. This implicates a potential strategy for the design of R
 NA-based targeted drugs.\n \n
LOCATION:Room 215\, CRUK Cambridge Research Institute
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