TUSC3 loss enhances ovarian cancer malignancy by promoting the
ER stress response

a 2015

TUSC3 loss enhances ovarian cancer malignancy by promoting the ER stress response

KRATOCHVÍLOVÁ, Kateřina, Peter HORAK, Michael KRAINER, Aleš HAMPL, Petr VAŇHARA et. al.

Základní údaje

Originální název

TUSC3 loss enhances ovarian cancer malignancy by promoting the ER stress response

Autoři

KRATOCHVÍLOVÁ, Kateřina, Peter HORAK, Michael KRAINER, Aleš HAMPL a Petr VAŇHARA

Vydání

Frontiers in material and life sciences: Creating life in 3D, 2015

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakt

Obor

10600 1.6 Biological sciences

Stát vydavatele

Česká republika

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Organizační jednotka

Lékařská fakulta

Klíčová slova česky

TUSC3, ovariální karcinom, stres ER, endoplazmatické retikulum, epiteliálně-mezenchymální tranzice

Klíčová slova anglicky

TUSC3, ovarian cancer, ER stress, endoplasmic reticulum, epithelial-to-mesenchymal transition, EMT

Příznaky

Mezinárodní význam

Změněno: 7. 10. 2015 11:32, Mgr. Kateřina Vašíčková, Ph.D.

Anotace

V originále

Ovarian cancer (OC) is one of the most serious cancers in women and despite recent progress in diagnosis and therapy, the prognosis for patients with OC is unfavorable, mostly because of late diagnosis and lack of reliable prognostic and predictive biomarkers. Recently, we described that epigenetic silencing of TUSC3 correlates with poor overall and disease-free survival of OC patients. TUSC3 is a putative tumor suppressor located in the membrane of endoplasmic reticulum (ER) participating in protein N-glycosylation. It is well established, that disturbances in N-glycosylation are associated with cancer development, however, the precise molecular mechanism, including the role of TUSC3, remains unclear. In our model, TUSC3 loss enhanced growth of OC cells in mice confirming the status of TUSC3 as a tumor suppressor, moreover, it altered ER stress response and promoted epithelial-to-mesenchymal transition in OC cells. In addition, TUSC3 downregulation resulted in earlier formation of 3D spheroids under low-adhesion condition and provided resistance to N-glycosylation inhibition-induced decomposition of spheroids. We conclude, that the cumulative effect of TUSC3 silencing and extrinsic signals triggering the ER stress response contributes to EMT and tumor dissemination as well as tumor progression in OC.

Návaznosti

MUNI/A/1558/2014, interní kód MU

Název: Zdroje pro tkáňové inženýrství 5 (Akronym: TissueEng5)

Investor: Masarykova univerzita, Zdroje pro tkáňové inženýrství 5, DO R. 2020_Kategorie A - Specifický výzkum - Studentské výzkumné projekty

MUNI/M/1050/2013, interní kód MU

Název: Automatizovaná analýza elektronmikroskopických snímků pro použití v biologii a medicíně (Akronym: Analýza TEM snímků)

Investor: Masarykova univerzita, Automatizovaná analýza elektronmikroskopických snímků pro použití v biologii a medicíně, INTERDISCIPLINARY - Mezioborové výzkumné projekty

Citovat

KRATOCHVÍLOVÁ, Kateřina, Peter HORAK, Michael KRAINER, Aleš HAMPL a Petr VAŇHARA. TUSC3 loss enhances ovarian cancer malignancy by promoting the ER stress response. In Frontiers in material and life sciences: Creating life in 3D. 2015.

@proceedings{1310356,
   author = {Kratochvílová, Kateřina and Horak, Peter and Krainer, Michael and Hampl, Aleš and Vaňhara, Petr},
   booktitle = {Frontiers in material and life sciences: Creating life in 3D},
   keywords = {TUSC3, ovarian cancer, ER stress, endoplasmic reticulum, epithelial-to-mesenchymal transition, EMT},
   language = {eng},
   title = {TUSC3 loss enhances ovarian cancer malignancy by promoting the ER stress response},
   url = {http://www.ceitec.eu/a5-abstracts-book-3d-finals/f33097},
   year = {2015}
}

TY  - CONF
ID  - 1310356
AU  - Kratochvílová, Kateřina - Horak, Peter - Krainer, Michael - Hampl, Aleš - Vaňhara, Petr
PY  - 2015
TI  - TUSC3 loss enhances ovarian cancer malignancy by promoting the ER stress response
KW  - TUSC3, ovarian cancer, ER stress, endoplasmic reticulum, epithelial-to-mesenchymal transition, EMT
UR  - http://www.ceitec.eu/a5-abstracts-book-3d-finals/f33097
N2  - Ovarian cancer (OC) is one of the most serious cancers in women and despite recent progress in diagnosis and therapy, the prognosis for patients with OC is unfavorable, mostly because of late diagnosis and lack of reliable prognostic and predictive biomarkers. Recently, we described that epigenetic silencing of TUSC3 correlates with poor overall and disease-free survival of OC patients. TUSC3 is a putative tumor suppressor located in the membrane of endoplasmic reticulum (ER) participating in protein N-glycosylation. It is well established, that disturbances in N-glycosylation are associated with cancer development, however, the precise molecular mechanism, including the role of TUSC3, remains unclear. In our model, TUSC3 loss enhanced growth of OC cells in mice confirming the status of TUSC3 as a tumor suppressor, moreover, it altered ER stress response and promoted epithelial-to-mesenchymal transition in OC cells. In addition, TUSC3 downregulation resulted in earlier formation of 3D spheroids under low-adhesion condition and provided resistance to N-glycosylation inhibition-induced decomposition of spheroids. We conclude, that the cumulative effect of TUSC3 silencing and extrinsic signals triggering the ER stress response contributes to EMT and tumor dissemination as well as tumor progression in OC.
ER  -

KRATOCHVÍLOVÁ, Kateřina, Peter HORAK, Michael KRAINER, Aleš HAMPL a Petr VAŇHARA. TUSC3 loss enhances ovarian cancer malignancy by promoting the ER stress response. In \textit{Frontiers in material and life sciences: Creating life in 3D}. 2015.

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