Autophagy modification augmented the treatment effects initiated by arsenic trioxide in NB4 cells.
Autophagy is a survival pathway required for cellular viability during starvation through catabolic self-digestion of damaged proteins and organelles; however, autophagy may result in cell death if it proceeds to completion. Although the exact mechanism of this process is not clear, it seems that proper regulation of autophagy can potentially contribute to the therapeutics of cancers. This study was designed to examine the role of autophagy in the death of human acute promyelocytic leukemia NB4 cells initiated by arsenic trioxide. Furthermore, the effects of autophagy inhibition and augmentation on cell viability were also compared. Our data suggested that both augmentation and suppression of autophagy could enhance the treatment effects while the latter was preferable. This study indicated that autophagy regulation augmented the treatment effects initiated by arsenic trioxide in NB4 cells, and that the selection of regulator should be precisely considered.
Ren
YaLi
Y
Lab of Electron Microscopy, Peking University First Hospital, No 8 Xishiku Street, XiCheng District, 100034 Beijing, China. guiling9893@sina.com
Xie
YanLing
Y
Chai
LiJun
L
Wang
ShuHe
S
Cheng
Ming
M
D000225:Adenine / Q000031:analogs & derivatives / Q000494:pharmacology; D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology*; D001343:Autophagy / Q000187:drug effects*; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D005434:Flow Cytometry; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D010087:Oxides / Q000494:pharmacology*; D020123:Sirolimus / Q000494:pharmacology
D000903:Antibiotics, Antineoplastic; D001152:Arsenicals; D010087:Oxides; C025946:3-methyladenine; D000225:Adenine; D000077237:Arsenic Trioxide; D020123:Sirolimus