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@article{1334095,
author = {Balvan, Jan and Gumulec, Jaromír and Raudenská, Martina and Krizova, Aneta and Štěpka, Petr and Babula, Petr and Kizek, René and Adam, Vojtech and Masařík, Michal},
article_location = {San Francisco},
article_number = {12},
doi = {http://dx.doi.org/10.1371/journal.pone.0145016},
keywords = {CONTROLLED HOLOGRAPHIC MICROSCOPE; HUMAN SOMATIC-CELLS; NF-KAPPA-B; UP-REGULATION; TUMOR PROGRESSION; INDUCED MITOPHAGY; FLOW-CYTOMETRY; LIVING CELLS; STEM-CELLS; AUTOPHAGY},
language = {eng},
issn = {1932-6203},
journal = {Plos one},
title = {Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating},
volume = {10},
year = {2015}
}
TY - JOUR
ID - 1334095
AU - Balvan, Jan - Gumulec, Jaromír - Raudenská, Martina - Krizova, Aneta - Štěpka, Petr - Babula, Petr - Kizek, René - Adam, Vojtech - Masařík, Michal
PY - 2015
TI - Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating
JF - Plos one
VL - 10
IS - 12
SP - 1-23
EP - 1-23
PB - Public Library of Science
SN - 19326203
KW - CONTROLLED HOLOGRAPHIC MICROSCOPE
KW - HUMAN SOMATIC-CELLS
KW - NF-KAPPA-B
KW - UP-REGULATION
KW - TUMOR PROGRESSION
KW - INDUCED MITOPHAGY
KW - FLOW-CYTOMETRY
KW - LIVING CELLS
KW - STEM-CELLS
KW - AUTOPHAGY
N2 - Resistant 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 cellcell 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.
ER -
BALVAN, Jan, Jaromír GUMULEC, Martina RAUDENSKÁ, Aneta KRIZOVA, Petr ŠTĚPKA, Petr BABULA, René KIZEK, Vojtech ADAM and Michal MASAŘÍK. Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating. \textit{Plos one}. San Francisco: Public Library of Science, 2015, vol.~10, No~12, p.~1-23. ISSN~1932-6203. Available from: https://dx.doi.org/10.1371/journal.pone.0145016.
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