Distinct phenotypes and ´bystander' effects of senescent tumour cells induced by docetaxel or immunomodulatory cytokines
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F18%3A00502293" target="_blank" >RIV/68378050:_____/18:00502293 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.3892/ijo.2018.4553" target="_blank" >http://dx.doi.org/10.3892/ijo.2018.4553</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3892/ijo.2018.4553" target="_blank" >10.3892/ijo.2018.4553</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Distinct phenotypes and ´bystander' effects of senescent tumour cells induced by docetaxel or immunomodulatory cytokines
Popis výsledku v původním jazyce
Cellular senescence is the process of the permanent proliferative arrest of cells in response to various inducers. It is accompanied by typical morphological changes, in addition to the secretion of bioactive molecules, including proinflammatory cytokines and chemokines [known as the senescence-associated secretory phenotype (SASP)]. Thus, senescent cells may affect their local environment and induce a so-called bystander' senescence through the state of SASP. The phenotypes of senescent cells are determined by the type of agent inducing cellular stress and the cell lineages. To characterise the phenotypes of senescent cancer cells, two murine cell lines were employed in the present study: TC-1 and B16F10 (B16) cells. Two distinct senescence inductors were used: Chemotherapeutic agent docetaxel (DTX) and a combination of immunomodulatory cytokines, including interferon (IFN) and tumour necrosis factor (TNF). It was demonstrated that DTX induced senescence in TC-1 and B16 tumour cell lines, which was demonstrated by growth arrest, positivegalactosidase staining, increased p21(Waf1) (p21) expression and the typical SASP capable of inducing a bystander' senescence. By contrast, treatment with a combination of T helper cell 1 cytokines, IFN and TNF, induced proliferation arrest only in B16 cells. Despite the presence of certain characteristic features resembling senescent cells (proliferation arrest, morphological changes and increased p21 expression), these cells were able to form tumours in vivo and started to proliferate upon cytokine withdrawal. In addition, B16 cells were not able to induce a bystander' senescence. In summary, the present study described cell line- and treatment- associated differences in the phenotypes of senescent cells that may be relevant in optimization of cancer chemo- and immunotherapy.
Název v anglickém jazyce
Distinct phenotypes and ´bystander' effects of senescent tumour cells induced by docetaxel or immunomodulatory cytokines
Popis výsledku anglicky
Cellular senescence is the process of the permanent proliferative arrest of cells in response to various inducers. It is accompanied by typical morphological changes, in addition to the secretion of bioactive molecules, including proinflammatory cytokines and chemokines [known as the senescence-associated secretory phenotype (SASP)]. Thus, senescent cells may affect their local environment and induce a so-called bystander' senescence through the state of SASP. The phenotypes of senescent cells are determined by the type of agent inducing cellular stress and the cell lineages. To characterise the phenotypes of senescent cancer cells, two murine cell lines were employed in the present study: TC-1 and B16F10 (B16) cells. Two distinct senescence inductors were used: Chemotherapeutic agent docetaxel (DTX) and a combination of immunomodulatory cytokines, including interferon (IFN) and tumour necrosis factor (TNF). It was demonstrated that DTX induced senescence in TC-1 and B16 tumour cell lines, which was demonstrated by growth arrest, positivegalactosidase staining, increased p21(Waf1) (p21) expression and the typical SASP capable of inducing a bystander' senescence. By contrast, treatment with a combination of T helper cell 1 cytokines, IFN and TNF, induced proliferation arrest only in B16 cells. Despite the presence of certain characteristic features resembling senescent cells (proliferation arrest, morphological changes and increased p21 expression), these cells were able to form tumours in vivo and started to proliferate upon cytokine withdrawal. In addition, B16 cells were not able to induce a bystander' senescence. In summary, the present study described cell line- and treatment- associated differences in the phenotypes of senescent cells that may be relevant in optimization of cancer chemo- and immunotherapy.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2018
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
International Journal of Oncology
ISSN
1019-6439
e-ISSN
—
Svazek periodika
53
Číslo periodika v rámci svazku
5
Stát vydavatele periodika
GR - Řecká republika
Počet stran výsledku
13
Strana od-do
1997-2009
Kód UT WoS článku
000447703300014
EID výsledku v databázi Scopus
—