ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium

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.

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

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.