KRATOCHVÍLOVÁ, Kateřina, Lukáš MORÁŇ, Cristina FONT CALVARONS, Ivana BALTASOVÁ, Aleš HAMPL and Petr VAŇHARA. ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium. In 12th International Congress of Cell Biology, Programme & Abstract Book. 2016.
Other formats:   BibTeX LaTeX RIS
Basic information
Original name ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium
Name (in English) ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium
Authors KRATOCHVÍLOVÁ, Kateřina, Lukáš MORÁŇ, Cristina FONT CALVARONS, Ivana BALTASOVÁ, Aleš HAMPL and Petr VAŇHARA.
Edition 12th International Congress of Cell Biology, Programme & Abstract Book, 2016.
Other information
Type of outcome Conference abstract
Confidentiality degree is not subject to a state or trade secret
WWW URL
Keywords (in Czech) stres endoplazmatického retikula, senescence, ovariální epitel, epiteliálně-mezenchymální tranzice
Keywords in English endoplasmic reticulum stress, ER stress, UPR, senescence, ovarian surface epithelium, epithelial-to-mesenchymal transition, EMT
Tags International impact
Changed by Changed by: Mgr. Kateřina Vašíčková, Ph.D., učo 356999. Changed: 29/7/2016 10:35.
Abstract
Endoplasmic reticulum (ER) is a multifunctional organelle primarily responsible for protein synthesis and folding. Disruption of ER function triggers a protective machinery called the unfolded protein response (UPR). UPR pathways then arrest the RNA translation and increase the production of ER chaperones to alleviate ER stress, or, if the stress cannot be resolved, UPR induces phenotypic change and/or apoptosis. Cellular senescence is a complex cell phenotype, whereby cells irreversibly cease to divide after a number of passages. It can be induced by telomere shortening, DNA damage, oxidative stress and activation of some oncogenes. Senescent cells accumulate with age in tissues and are assumed to play a role in age-associated diseases, such as Alzheimer disease or cancer. In our work, induction of senescence lead to upregulation of UPR hallmark proteins and interestingly, alleviation of ER stress by inhibition of UPR signaling or by chemical chaperons, overridden the onset of senescence. In summary, these results indicate a biologically relevant link between UPR and senescence of OSE cells that may contribute to better understanding of ovarian pathologies extending the portfolio of druggable molecular targets.
Abstract (in English)
Endoplasmic reticulum (ER) is a multifunctional organelle primarily responsible for protein synthesis and folding. Disruption of ER function triggers a protective machinery called the unfolded protein response (UPR). UPR pathways then arrest the RNA translation and increase the production of ER chaperones to alleviate ER stress, or, if the stress cannot be resolved, UPR induces phenotypic change and/or apoptosis. Cellular senescence is a complex cell phenotype, whereby cells irreversibly cease to divide after a number of passages. It can be induced by telomere shortening, DNA damage, oxidative stress and activation of some oncogenes. Senescent cells accumulate with age in tissues and are assumed to play a role in age-associated diseases, such as Alzheimer disease or cancer. In our work, induction of senescence lead to upregulation of UPR hallmark proteins and interestingly, alleviation of ER stress by inhibition of UPR signaling or by chemical chaperons, overridden the onset of senescence. In summary, these results indicate a biologically relevant link between UPR and senescence of OSE cells that may contribute to better understanding of ovarian pathologies extending the portfolio of druggable molecular targets.
PrintDisplayed: 5/3/2024 16:18