Effect of Emodin Combined with AZT on the Proliferation and the Expression of BCL-2, NF-κB, TGF-β in the Leukemia Stem Cells-KG-1a cells.
- Author:
Li-Na WANG
1
;
Zi-Jian LI
1
;
Ya-Ming XI
2
;
Che CHEN
3
;
Ting MA
1
;
Li ZHAO
1
;
Ming-Feng JIA
1
;
Ming LI
1
;
Hao ZHANG
1
;
Chun-Xia LIU
1
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Emodin; pharmacology; Humans; Leukemia; NF-kappa B p50 Subunit; metabolism; Neoplastic Stem Cells; cytology; drug effects; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; Transforming Growth Factor beta1; metabolism; Zidovudine; pharmacology
- From: Journal of Experimental Hematology 2015;23(5):1265-1271
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of Emodin combined with 3'-azido-3'-deoxythymidine (AZT) on the proliferation and apoptosis of concentrated leukemia stem cells (CLSC)-human acute myeloid leukemia KG-la cells and expression of BCL-2, NF-κB and TGF-β.
METHODSThe tumor stem cell-like subpopulation in human leukemia cell line KG-1a was enriched with 5-fluorouracil (5-FU). The CD34⁺ CD38⁻ subpopulation in the KG-1a cells was detected with flow cytometry, the cell proliferation was detected by MTT method to study the of Emodin and AZT in the CLSC. The cell apoptosis was analyzed by flow cytometry. The expression of NF-κB, BCL-2 and TGF-β mRNA and proteins were measured with RT-PCR and Western blot respectively.
RESULTSAs compared with cells treated with mentioned above drugs alone, the inhibition of proliferation potential and apoptosis rate of cells in combination group markedly increase with time and concentration dependent member (P < 0.01), the expression of NF-κB, BCL-2 and TGF-β mRNA and proteins decreased.
CONCLUSIONEmodin combined AZT can synergistically inhibit the proliferation, induce cell apoptosis, and down regulate the expression of NF-κB, BCL-2 and TGF-β mRNA and proteins in the CLSC, the possible mechanism of synergistic effect may be associated with inhibiton of BCL-2 activation and down-regulation of the expression of NF-κB, and TGF-β.