ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium

KRATOCHVÍLOVÁ, Kateřina, Lukáš MORÁŇ, Cristina FONT CALVARONS, Ivana BALTASOVÁ, Aleš HAMPL a Petr VAŇHARA. ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium. In 12th International Congress of Cell Biology, Programme & Abstract Book. 2016.

Základní údaje

• Originální název: ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium
• Název anglicky: ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium
• Autoři: KRATOCHVÍLOVÁ, Kateřina, Lukáš MORÁŇ, Cristina FONT CALVARONS, Ivana BALTASOVÁ, Aleš HAMPL a Petr VAŇHARA.
• Vydání: 12th International Congress of Cell Biology, Programme & Abstract Book, 2016.

Další údaje

• Typ výsledku: Konferenční abstrakt
• Utajení: není předmětem státního či obchodního tajemství
• WWW: URL
• Klíčová slova česky: stres endoplazmatického retikula, senescence, ovariální epitel, epiteliálně-mezenchymální tranzice
• Klíčová slova anglicky: endoplasmic reticulum stress, ER stress, UPR, senescence, ovarian surface epithelium, epithelial-to-mesenchymal transition, EMT
• Příznaky: Mezinárodní význam

Anotace

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.

Anotace anglicky

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.