Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating

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dc.contributor.authorBalvan, Jancs
dc.contributor.authorGumulec, Jaromírcs
dc.contributor.authorRaudenská, Martinacs
dc.contributor.authorKřížová, Anetacs
dc.contributor.authorŠtěpka, Petrcs
dc.contributor.authorBabula, Petrcs
dc.contributor.authorKizek, Renécs
dc.contributor.authorAdam, Vojtěchcs
dc.contributor.authorMasařík, Michalcs
dc.coverage.issue12cs
dc.coverage.volume10cs
dc.date.accessioned2020-08-04T11:04:05Z
dc.date.available2020-08-04T11:04:05Z
dc.date.issued2015-12-15cs
dc.description.abstractResistant cancer phenotype is a key obstacle in the successful therapy of prostate cancer. The primary aim of our study was to explore resistance mechanisms in the advanced type of prostate cancer cells (PC-3) and to clarify the role of autophagy in these processes. We performed time-lapse experiment (48 hours) with ROS generating plumbagin by using multimodal holographic microscope. Furthermore, we also performed the flow-cytometric analysis and the qRT-PCR gene expression analysis at 12 selected time points. TEM and confocal microscopy were used to verify the results. We found out that autophagy (namely mitophagy) is an important resistance mechanism. The major ROS producing mitochondria were coated by an autophagic membrane derived from endoplasmic reticulum and degraded. According to our results, increasing ROS resistance may be also accompanied by increased average cell size and polyploidization, which seems to be key resistance mechanism when connected with an escape from senescence. Many different types of cell-cell interactions were recorded including entosis, vesicular transfer, eating of dead or dying cells, and engulfment and cannibalism of living cells. Entosis was disclosed as a possible mechanism of polyploidization and enabled the long-term survival of cancer cells. Significantly reduced cell motility was found after the plumbagin treatment. We also found an extensive induction of pluripotency genes expression (NANOG, SOX2, and POU5F1) at the time-point of 20 hours. We suppose, that overexpression of pluripotency genes in the portion of prostate tumour cell population exposed to ROS leads to higher developmental plasticity and capability to faster respond to changes in the extracellular environment that could ultimately lead to an alteration of cell fate.en
dc.description.abstractFenotyp rezistentní rakoviny představuje hlavní překážku v úspěšné léčbě rakoviny prostaty. Primárním cílem naší studie bylo prozkoumat mechanismy rezistence v pokročilém druhu rakovinných buněk prostaty (PC-3) a objasnit roli autofagie v tomto procesu.cs
dc.formattextcs
dc.format.extent1-23cs
dc.format.mimetypeapplication/pdfcs
dc.identifier.citationPLOS ONE. 2015, vol. 10, issue 12, p. 1-23.en
dc.identifier.doi10.1371/journal.pone.0145016cs
dc.identifier.issn1932-6203cs
dc.identifier.other121090cs
dc.identifier.urihttp://hdl.handle.net/11012/63726
dc.language.isoencs
dc.publisherPLOScs
dc.relation.ispartofPLOS ONEcs
dc.relation.urihttp://europepmc.org/articles/PMC4679176?pdf=rendercs
dc.rightsCreative Commons Attribution 4.0 Internationalcs
dc.rights.accessopenAccesscs
dc.rights.sherpahttp://www.sherpa.ac.uk/romeo/issn/1932-6203/cs
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/cs
dc.subjectOxidativní stres; rakovina prostaty
dc.subjectholografická mikroskopie
dc.subjectOxidative stressen
dc.subjectprostate canceren
dc.subjectholographic microscopyen
dc.titleOxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eatingen
dc.title.alternativeRezistence vůči oxidačnímu stresu metastatického karcinomu prostaty: Obnovování samopojídánímcs
dc.type.driverarticleen
dc.type.statusPeer-revieweden
dc.type.versionpublishedVersionen
sync.item.dbidVAV-121090en
sync.item.dbtypeVAVen
sync.item.insts2020.08.04 13:04:04en
sync.item.modts2020.08.04 12:35:08en
thesis.grantorVysoké učení technické v Brně. Středoevropský technologický institut VUT. Experimentální biofotonikacs
thesis.grantorVysoké učení technické v Brně. Středoevropský technologický institut VUT. Chytré nanonástrojecs
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