Összesen 1 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM107571
Első szerző:Jambrovics Károly (biológus, gyógyszer-biotechnológus)
Cím:ATRA and ATO combination has several beneficial effects in treatment of Acute Promyelocytic Leukaemia cells / Jambrovics Károly, Balajthy Zoltán
Dátum:2022
Megjegyzések:All-trans-retinoic acid (ATRA) therapy is one of the most frequently used therapy to treat acute promyelocyte leukaemia (APL) inducing terminal differentiation towards neutrophil granulocytes. Arsenic-trioxide (ATO) and ATRA and ATO combined treatments had been identified as another effective treatment in the late 90s' and then it was subsequently proved that this therapy can trigger both inductions of apoptosis and attenuation the inflammatory cytokine/chemokine production in vitro [Jambrovics et al., Cancer 2020]. Combined treatments can prolong the survival of APL patients in a dose-dependent manner by activation of the cellular signalling pathways leading to, among others, an enhanced reactive oxygen species (ROS) generation by the NADPH-oxidase system. ATO alone induces partial differentiation and apoptosis, leading to the remission in relapsed APL patients with the initiation of the degradation of the PML-RAR? oncoprotein. ATRA and ATO combined treatments result in up and down-regulation of more than a thousand genes to generate functional neutrophil granulocytes. One of the most up-regulated genes in ATRA induced differentiation of NB4 APL cell line is the tissue transglutaminase (TG2). Silencing and knocking out of TG2 expression in NB4 cells revealed that TG2 is required for adhesion, migratory, the phagocytic capacity of neutrophils, superoxide (ROS) production and inflammatory cytokine/chemokine production [Balajthy et al., Blood 2006, Jambrovics et al., Haematologica 2018, Jambrovics et al., Cancer 2020]. To investigate the role of TG2 further, NB4 cell lines were treated with ATRA + ATO in two different combinations, where we found that without the TG2, NB4 cells were more sensitive to the arsenic-induced apoptosis. Additionally, we observed that the apoptosis induction by arsenic resulted in a degradation of the TG2 protein.
Tárgyszavak:Orvostudományok Elméleti orvostudományok előadáskivonat
könyvrészlet
Megjelenés:15th Molecular, Cell and Immune Biology Winter Symposium : Book of abstract. - p. 25
További szerzők:Balajthy Zoltán (1957-) (biokémikus, sejtbiológus)
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1