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Apoptotic effect of As2S2 on K562 cells and its mechanism.

	author = {Jun-E LI and Wwi-Li WU and Zhen-Yi WANG and Guan-Lin SUN},
	title = {Apoptotic effect of As2S2 on K562 cells and its mechanism.},
	journal = {Acta Pharmacologica Sinica},
	volume = {23},
	number = {11},
	year = {2016},
	keywords = {},
	abstract = {AIM: To investigate the apoptotic effect of As2S2 on K562 cells and its
METHODS: The effect of As2S2 on proliferation of K562 cells was determined by
counting the number of cells. Apoptosis was assessed by flow cytometry, DNA
fragmentation analysis, and morphology observation. Expression of protein was
determined by Western blot. RT-PCR was used to evaluate changes in gene
RESULTS: As2S2 greatly inhibited the proliferation and induced apoptosis of K562 
cells in a concentration- and time-dependent manner at the concentration range of
1-5 micromol/L during 24-72 h. Viable cells were decreased to approximately 71 % 
of control at the concentration of 5 micromol/L after 48-h incubation, 31.4 %
after 72-h incubation, and 45.4 % at 3 micromol/L after 72-h incubation. At 3
micromol/L for 72 h, 5 micromol/L for 48 h, and 5 micromol/L for 72 h, the
apoptosis rate were 34.4 %, 21.8 %, and 46 % of the treated-cells, respectively. 
As2S2 decreased the Bcr-Abl fusion protein and protein tyrosine kinase (PTK)
activity of c-abl and Bcr-Abl, but it did not change the transcription of bcr-abl
assayed. As2S2 also induced apoptosis in fresh mononuclear cells derived from
chronic myelogenous leukemia (CML) patients. CML Ph+ leukemia cells were more
sensitive to the apoptotic effect of As2S2 than Ph- mononuclear cells (P},
	issn = {1745-7254},	url = {}