Endoplasmic Reticulum stress signaling in cancer
Event details
| Date | 09.05.2016 |
| Hour | 15:00 › 16:00 |
| Speaker |
Dr. Eric Chevet Oncogenesis, Stress & Signaling Laboratory, University of Rennes, France http://oss-clcc-rennes.com/research/group2/people.html |
| Location | |
| Category | Conferences - Seminars |
Growing evidences support the contribution of the Unfolded Protein Response (UPR) to tumor growth. However the molecular mechanisms underlying remain poorly understood. We recently found that the endoplasmic reticulum stress sensor IRE1alpha was capable of selectively controlling cancer cell fate in vitro and in vivo through its endoribonuclease activity, mechanism named Regulated IRE1-Dependent RNA Decay (RIDD). We demonstrated that RIDD activity controls cancer cell adaptation and tumor development. Indeed inhibition of IRE1alpha signaling prevented the degradation of select RNAs, thereby sensitizing cells to stress, altering tumorigenesis and mouse survival following orthotopic implantation of glioma cells. In contrast, silencing specific RIDD substrates components in IRE1alpha deficient cells restored select properties of tumor growth in vivo. Tumor analyses revealed that low RIDD substrate expression correlated with high IRE1alpha activity and poor patient survival. Moreover, we recently showed that IRE1alpha expression levels are also controlled through post-translational mechanisms involving small non-coding RNAs, thereby adding to the repertoire of UPR-mediated control of tumor development. Thus, our data identify novel mechanisms connecting the UPR and small non-coding RNA through post-transcriptional mechanisms in tumor cells. This highlights the importance of this interplay in cancer cell survival advantage and tumor development.
Practical information
- Informed public
- Free
Organizer
- Prof. Gisou van der Goot
Contact
- Geneviève Rossier [email protected]