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SUMMARY:Endoplasmic Reticulum stress signaling in cancer
DTSTART:20160509T150000
DTEND:20160509T160000
DTSTAMP:20260427T215422Z
UID:2f01881286f3e0ab48f71a38cbd03d2bcc8cf16905424c877a4b2b7f
CATEGORIES:Conferences - Seminars
DESCRIPTION:Dr. Eric Chevet\nOncogenesis\, Stress & Signaling Laboratory\,
  University of Rennes\, Francehttp://oss-clcc-rennes.com/research/group2/p
 eople.html\nGrowing evidences support the contribution of the Unfolded Pro
 tein Response (UPR) to tumor growth. However the molecular mechanisms unde
 rlying remain poorly understood. We recently found that the endoplasmic re
 ticulum stress sensor IRE1alpha was capable of selectively controlling can
 cer cell fate in vitro and in vivo through its endoribonuclease activity\,
  mechanism named Regulated IRE1-Dependent RNA Decay (RIDD). We demonstrate
 d that RIDD activity controls cancer cell adaptation and tumor development
 . Indeed inhibition of IRE1alpha signaling prevented the degradation of se
 lect RNAs\, thereby sensitizing cells to stress\, altering tumorigenesis a
 nd mouse survival following orthotopic implantation of glioma cells. In co
 ntrast\, silencing specific RIDD substrates components in IRE1alpha defici
 ent cells restored select properties of tumor growth in vivo. Tumor analys
 es revealed that low RIDD substrate expression correlated with high IRE1al
 pha activity and poor patient survival. Moreover\, we recently showed that
  IRE1alpha expression levels are also controlled through post-translationa
 l mechanisms involving small non-coding RNAs\, thereby adding to the reper
 toire of UPR-mediated control of tumor development. Thus\, our data identi
 fy novel mechanisms connecting the UPR and small non-coding RNA through po
 st-transcriptional mechanisms in tumor cells. This highlights the importan
 ce of this interplay in cancer cell survival advantage and tumor developme
 nt.
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STATUS:CONFIRMED
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