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Statements

Subject Item
n2:RIV%2F00216208%3A11310%2F14%3A10284445%21RIV15-MSM-11310___
rdf:type
skos:Concept n16:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.4149/neo_2014_050
dcterms:description
The most common malignancies of the female genital tract are endometrial carcinomas, whose are generally proceeded by hyperplasia. The maintenance of tissue homeostasis is to great extent governed by apoptosis, whose defects can lead to the preneoplastic and/or cancerous changes. Endometrial apoptosis involves among others three groups of proteins of the Bcl-2 family. First group contains anti-apoptotic proteins (e. g. Bcl-2, Bcl-xL). The other two groups belong to the pro-apoptotic proteins with three (e. g. Bax, Bak) or one (e. g. Bad, Bid) so-called BH domains. Bad and Bid trigger the oligomerization of Bak and Ban protein, which permeabilize the outer mitochondrial wall. Unlike Bid, Bad cannot directly trigger apoptosis. Instead, Bad lowers the threshold at which apoptosis is induced, by binding anti-apoptotic Bcl-2 proteins. However, their mutual counterbalance or synergism in the human endometrium has not been reported yet. In this study, the levels of Bid and Bad were measured using SDS-PAGE and Western blotting with specific antibodies, with the aim to analyse expression of Bid and Bad proteins in normal (NE), hyperplastic (HE) and cancerous (CE) endometrium. We demonstrated that Bid expression in CE reached only 47% and 50% of this observed in NE and HE. Conversely, Bad expression in HE reached only 40% and 36% of this observed in NE and CE, respectively. We detected no significant changes of Bid expression between HE and NE, and levels of Bad protein were not different between CE and NE. Trend of Bid and Bad protein expression is clearly opposite in HE and CE. We hypothesise that disrupted apoptotic program in CE seems to be reduced further by lowering levels of direct apoptotic trigger protein Bid. We suggest that the adenocarcinoma tissue of human endometrium thus tries to strengthen its apoptotic effort by lowering the apoptotic threshold via higher Bad levels. The most common malignancies of the female genital tract are endometrial carcinomas, whose are generally proceeded by hyperplasia. The maintenance of tissue homeostasis is to great extent governed by apoptosis, whose defects can lead to the preneoplastic and/or cancerous changes. Endometrial apoptosis involves among others three groups of proteins of the Bcl-2 family. First group contains anti-apoptotic proteins (e. g. Bcl-2, Bcl-xL). The other two groups belong to the pro-apoptotic proteins with three (e. g. Bax, Bak) or one (e. g. Bad, Bid) so-called BH domains. Bad and Bid trigger the oligomerization of Bak and Ban protein, which permeabilize the outer mitochondrial wall. Unlike Bid, Bad cannot directly trigger apoptosis. Instead, Bad lowers the threshold at which apoptosis is induced, by binding anti-apoptotic Bcl-2 proteins. However, their mutual counterbalance or synergism in the human endometrium has not been reported yet. In this study, the levels of Bid and Bad were measured using SDS-PAGE and Western blotting with specific antibodies, with the aim to analyse expression of Bid and Bad proteins in normal (NE), hyperplastic (HE) and cancerous (CE) endometrium. We demonstrated that Bid expression in CE reached only 47% and 50% of this observed in NE and HE. Conversely, Bad expression in HE reached only 40% and 36% of this observed in NE and CE, respectively. We detected no significant changes of Bid expression between HE and NE, and levels of Bad protein were not different between CE and NE. Trend of Bid and Bad protein expression is clearly opposite in HE and CE. We hypothesise that disrupted apoptotic program in CE seems to be reduced further by lowering levels of direct apoptotic trigger protein Bid. We suggest that the adenocarcinoma tissue of human endometrium thus tries to strengthen its apoptotic effort by lowering the apoptotic threshold via higher Bad levels.
dcterms:title
Bad and Bid - potential background players in preneoplastic to neoplastic shift in human endometrium Bad and Bid - potential background players in preneoplastic to neoplastic shift in human endometrium
skos:prefLabel
Bad and Bid - potential background players in preneoplastic to neoplastic shift in human endometrium Bad and Bid - potential background players in preneoplastic to neoplastic shift in human endometrium
skos:notation
RIV/00216208:11310/14:10284445!RIV15-MSM-11310___
n3:aktivita
n18:Z n18:P n18:I
n3:aktivity
I, P(GAP207/12/0919), Z(MSM0021620858)
n3:cisloPeriodika
4
n3:dodaniDat
n9:2015
n3:domaciTvurceVysledku
n7:8184658 n7:6581102
n3:druhVysledku
n19:J
n3:duvernostUdaju
n17:S
n3:entitaPredkladatele
n4:predkladatel
n3:idSjednocenehoVysledku
4769
n3:idVysledku
RIV/00216208:11310/14:10284445
n3:jazykVysledku
n8:eng
n3:klicovaSlova
human endometrium; cancerogenesis; Bid; Bad
n3:klicoveSlovo
n5:Bid n5:human%20endometrium n5:Bad n5:cancerogenesis
n3:kodStatuVydavatele
SK - Slovenská republika
n3:kontrolniKodProRIV
[81121587B517]
n3:nazevZdroje
Neoplasma
n3:obor
n20:FK
n3:pocetDomacichTvurcuVysledku
2
n3:pocetTvurcuVysledku
6
n3:projekt
n12:GAP207%2F12%2F0919
n3:rokUplatneniVysledku
n9:2014
n3:svazekPeriodika
61
n3:tvurceVysledku
Halaška, Michael Bolehovská, Petra Novotný, Jiří Dvorská, Monika Švandová, Ivana Driák, Daniel
n3:wos
000342881700005
n3:zamer
n15:MSM0021620858
s:issn
0028-2685
s:numberOfPages
5
n13:doi
10.4149/neo_2014_050
n10:organizacniJednotka
11310