Dec 7, 2019

Acetylshikonin induces apoptosis of human leukemia cell line K562 by inducing S phase cell cycle arrest, modulating ROS accumulation, depleting Bcr-Abl and blocking NF-κB signaling

Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie
Gangping HaoZhongfa Yang

Abstract

Acetylshikonin, a natural naphthoquinone derivative compound from Lithospermum erythrorhyzon, has been reported to kill bacteria, suppress inflammation, and inhibit tumor growth. However, the effect of acetylshikonin on human chronic myelocytic leukemia (CML) cells apoptosis and its detailed mechanisms remains unknown. The purpose of the present study was to investigate whether acetylshikonin could inhibit proliferation or induce apoptosis of the K562 cells, and whether by regulating the NF-κB signaling pathway to suppress the development of CML. K562 cells were treated with serial diluted acetylshikonin at different concentrations. Our data showed that K562 cell growth was significantly inhibited by acetylshikonin with an IC50 of 2.03 μM at 24 h and 1.13 μM at 48 h, with increased cell cycle arrest in S-phase. The results of annexin V-FITC/PI and AO/EB staining showed that acetylshikonin induced cell apoptosis in a dose-dependent manner. K562 cells treated with acetylshikonin underwent massive apoptosis accompanied by a rapid generation of reactive oxygen species (ROS). Scavenging the ROS completely blocked the induction of apoptosis following acetylshikonin treatment. The levels of the pro-apoptotic proteins Bax, cleaved casp...Continue Reading

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Mentioned in this Paper

Caspase-9
Study
Cyclophosphamide
Annexin A5
Cleaved
Caspase-3
PARP1 protein, human
DDAH2
Cell Proliferation
NFKB Signaling Pathway

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis