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Statements

Subject Item
n2:RIV%2F00216208%3A11150%2F12%3A10123422%21RIV13-MSM-11150___
rdf:type
skos:Concept n10:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1016/j.tiv.2011.12.010
dcterms:description
Sodium selenite (Se) is known to induce diverse stress responses in malignant cells which may lead to various types of cell death including apoptosis and/or autophagy. In colon cancer cells, Se activates several signaling pathways whose interactions and ultimate endpoints may vary in individual study models. In our previous work we showed differences in Se-dependent growth inhibition, cell cycle alterations and apoptosis in colon cancer cells with functional (HCT-116) and deleted (HCT-116-p53KO) p53. Moreover, detailed morphological and biochemical analyses revealed the presence of autophagy in Se-treated cells. Thus the aim of this study was to investigate in detail mechanisms, relationship and crosstalk between apoptosis and autophagy in Se-treated HCT-116 cancer cells differing in p53 status since p53 has been shown to play a well-known role in apoptosis but dichotomous role in autophagy. We report that the absence of p53 in malignant colonocytes changes patterns of response to Se-induced stress which include differential activation of MAP kinases (p38 - HCT-116 and JNK - HCT-116 p53KO) including their respective roles in the process of apoptosis and autophagy as well as the involvement of mTOR or PI3K signaling. Our results seem to suggest that deletion of p53 inevitably leads to a higher level of instability and delays in an individual cell decision in the face of stress whether to activate apoptosis or autophagy which may consequently occur simultaneously with mutual dichotomous relationship. Sodium selenite (Se) is known to induce diverse stress responses in malignant cells which may lead to various types of cell death including apoptosis and/or autophagy. In colon cancer cells, Se activates several signaling pathways whose interactions and ultimate endpoints may vary in individual study models. In our previous work we showed differences in Se-dependent growth inhibition, cell cycle alterations and apoptosis in colon cancer cells with functional (HCT-116) and deleted (HCT-116-p53KO) p53. Moreover, detailed morphological and biochemical analyses revealed the presence of autophagy in Se-treated cells. Thus the aim of this study was to investigate in detail mechanisms, relationship and crosstalk between apoptosis and autophagy in Se-treated HCT-116 cancer cells differing in p53 status since p53 has been shown to play a well-known role in apoptosis but dichotomous role in autophagy. We report that the absence of p53 in malignant colonocytes changes patterns of response to Se-induced stress which include differential activation of MAP kinases (p38 - HCT-116 and JNK - HCT-116 p53KO) including their respective roles in the process of apoptosis and autophagy as well as the involvement of mTOR or PI3K signaling. Our results seem to suggest that deletion of p53 inevitably leads to a higher level of instability and delays in an individual cell decision in the face of stress whether to activate apoptosis or autophagy which may consequently occur simultaneously with mutual dichotomous relationship.
dcterms:title
Selenite-induced apoptosis and autophagy in colon cancer cells Selenite-induced apoptosis and autophagy in colon cancer cells
skos:prefLabel
Selenite-induced apoptosis and autophagy in colon cancer cells Selenite-induced apoptosis and autophagy in colon cancer cells
skos:notation
RIV/00216208:11150/12:10123422!RIV13-MSM-11150___
n10:predkladatel
n11:orjk%3A11150
n3:aktivita
n18:S n18:I
n3:aktivity
I, S
n3:cisloPeriodika
2
n3:dodaniDat
n13:2013
n3:domaciTvurceVysledku
n7:2168928 n7:8579687 n7:2650673 n7:1249746
n3:druhVysledku
n15:J
n3:duvernostUdaju
n4:S
n3:entitaPredkladatele
n14:predkladatel
n3:idSjednocenehoVysledku
167330
n3:idVysledku
RIV/00216208:11150/12:10123422
n3:jazykVysledku
n16:eng
n3:klicovaSlova
Autophagy; Apoptosis; Colon cancer; Sodium selenite
n3:klicoveSlovo
n6:Colon%20cancer n6:Sodium%20selenite n6:Apoptosis n6:Autophagy
n3:kodStatuVydavatele
NL - Nizozemsko
n3:kontrolniKodProRIV
[2D15DFC545D0]
n3:nazevZdroje
Toxicology in Vitro
n3:obor
n12:EB
n3:pocetDomacichTvurcuVysledku
4
n3:pocetTvurcuVysledku
4
n3:rokUplatneniVysledku
n13:2012
n3:svazekPeriodika
26
n3:tvurceVysledku
Benešová, Soňa Králová, Věra Červinka, Miroslav Rudolf, Emil
n3:wos
000301019600009
s:issn
0887-2333
s:numberOfPages
11
n19:organizacniJednotka
11150