期刊文献+

全反式维甲酸对K562细胞的诱导分化作用 被引量:1

Differentiation-Inducing Effect of ATRA on Leukemia Cell Line K562
暂未订购
导出
摘要 目的 全反式维甲酸(ATRA)对肿瘤细胞具有广泛的抑制增殖、促进分化作用。本研究通过体外培养检测ATRA对K562细胞是否具有诱导分化作用。方法 采用联苯胺染色、瑞氏染色、非特异性酯酶染色、硝基四唑氮蓝还原试验4种不同的染色方法及流式细胞术,观察经1μmol/L及2.5μmol/L ATRA诱导1d,4d,5d后,K562细胞出现诱导分化特征。结果 1μmol/L及2.5μmol/L ATRA均可诱导K562细胞向粒系分化。培养4d,1μmol/L ATRA组61.5%的K562细胞、2.5μmol/L组39%的K562细胞显示出向粒系成熟方向分化;培养5d,处理组的分化细胞数仍明显高于对照组(P<0.05),但两种浓度ATRA的诱导分化强度无统计学差异(P>0.05)。且均未出现向红系或单核细胞方向分化的特征。流式细胞仪检测ATRA诱导前后CD13及CD71的表达,1μmol/L ATRA诱导K562细胞1d,CD13抗原表达阳性率为8.0%,2.5μmol/L组则为6.7%,均高于对照组(2.1%)。培养5d,1μmol/L和2.5μmol/L AFRA组的CD13分别升高到28.1%,37.8%,而CD71则分别下降至1.2%和0.9%。与对照组比差异均具有显著性(P<0.05)。结论 ATRA可诱导K562细胞向粒系成熟方向分化。 Objective ATRA can restrain proliferation and promote differentiation in various tumor cells. The aim of the study is to investigate the differentiation characteristics of K562 induced by ATRA. Methods Morphology (Benzidine staining, Wright's staining, NSE staining and NBT recovery test) and flow cytometry were used to observe the differentiation characteristics of K562 after co-incubation with 1 μmol/L and 2.5 pmol/L ATRA for 1 d, 4 ds, and 5 ds. Results Co-incubated for 4 ds, 61.5% K562 cells in the 1 μmol/L ATRA group and 39% K562 cells in the 2.5 μmol/L ATRA group showed some evidence of myeloid maturation, but no evidence of erythroid or monocytoid maturation. Cb-incubated for 5 ds, the percentage of differentiated K562 cells was much higher than that in the control group. One day after induction by 1 μmol/L ATRA or 2.5 μmol/L ATRA, the expression of CD13 was 8.0% and 6.7%, respectively, which was higher than that in the control group (2.1%). Five days after induction by 1 μmol/L ATRA or 2.5 μmol/L ATRA, the expression of CD13 increased to 28.1 % and 37.8 % , respectively, while the expression of CD71 decreased to 1.2 % and 0.9 % respectively. The differences between the ATRA groups and the control group were significant ( P < 0.05). CD71 decreased from 9.7% and 10.8% in the 1 μmol/L and 2.5 μmol/L ATRA groups on day 1 to 1.2% and 0.9% on day 5, while the CD13 expression level increased from 8.0% and 6.7% to 28.1% and 37.8% , respectively. Conclusions ATRA can induce K562 to differentiate into myeloid linage. [Chin J Contemp Pediatr, 2003, 5(1): 8-11]
出处 《中国当代儿科杂志》 CAS CSCD 2003年第1期8-11,共4页 Chinese Journal of Contemporary Pediatrics
关键词 全反式维甲酸 白血病细胞 K562 诱导分化 ATRA Leukemic cell K562 Differentitation
  • 相关文献

参考文献8

  • 1[1]Niitsu N, Umeda M, Honma Y. Myeloid and monocytoid leukemia cells have different sensitivity to differentiation-inducing activity of deoxyadenosine analogs [J]. Leuk Res, 2000, 24(1): 1-9.
  • 2[2]Yamamoto-Yamaguchi Y, Okabe-Kado J, Kasukabe T, et al. Induction of differentiation of human myeloid leukemia cells by immunosuppressant macrolides (rapamycin and FK506) and calcium / calmodulin-dependent kinase inhibitors [J]. Exp Hematol, 2001, 29(5): 582-588.
  • 3[3]Strelkov LA, Mikhailova AA, Fonina LA, et al. A new endogenous differentiating factor (myelopeptide-4) for myeloid cells [J]. FEBS Lett, 2000, 470(3): 281-284.
  • 4[4]Breitmann TR, Selonick SE, Collins SJ. Introduction of differentiation of the human promyelocytic leukemia cell line (HL-60) by retinoic acid [J]. Proc Natl Acad Sci USA, 1980, 77(5): 2936-2940.
  • 5[5]Peter JA, James P, Basilous E, et al. Retinoids as generized regulators of cellular growth and differentiation [J]. Am J Med Sci, 1988, 296(3): 164-170.
  • 6[6]Bianchi N, Osti F, Rutigliano C, et al. The DNA-binding drugs mithramycin and chromomycin are powerful inducers of erythroid differentiation of human K562 cells [J]. Br J Haematol, 1999, 104(2): 258-265.
  • 7[7]Goplen DP, Brackman D, Aksnes L, et al. Effects of 1, 25-dihydroxyvitamin D3 and retinoic acid on the proliferation and cell cycle phase distribution of neuroblastoma SK-N-SH cells [J]. Pediatr Hematol Oncol, 1994, 11(2): 173-179.
  • 8[8]Aoki S, Higuchi K, Isozumi N, et al. Differentiation in chronic myelogenous leukemia cell K562 by spongean sesterterpene [J]. Biochem Biophys Res Commun, 2001, 282(2): 426-4310.

同被引文献12

  • 1孙蕾,高举,袁粒星,陈婷婷,潘玲丽,周晨燕,朱易萍.TPA诱导K562细胞分化过程中线粒体铁蛋白表达情况研究[J].中国实验血液学杂志,2007,15(2):272-277. 被引量:3
  • 2Levi S, Corsis B, Bosisio M, et al. A human mitochondrial ferritin encoded by an intronless gene. J Biol Chem, 2001 . 276 (27):24437-24440.
  • 3Drysdale J, Arosio P, Invernizzi R, et al. Mitoehondrial ferritin: a new player in iron metabolism. Blood Cells Mol Dis, 2002;29(3) :376-383.
  • 4Cazzola M, Skoda RC. Translational pathophysiology: a novelmolecular mechanism of human disease. Blood, 2000. 95 (11) :3280-3288.
  • 5Corsi B, Cozzi A, Arosio P, et al. Human mitoehondrial ferrltin expressed in HeLa cells incorporates iron and affects cellular iron metabolism. J Biol Chem, 2002 ; 277 (25) : 22430 - 22437.
  • 6Levi S, Arosio P, Mitochondrial ferritin Int J Biochem Cell Bioh 2004 ;36(10) : 1887-1889.
  • 7Cazzola M, Invernizzi R, Bergamasehi G, et al. Mitoehondrial ferrritin express in erythroid eells from patients with sideroblastic anemia. Blood, 2003 . 101 (5) : 1996-2000.
  • 8Napier I, Ponka P, Richardson DR. Iron trafficking in the mitochondria: novel pathways revealed by disease. Blood, 2005;105(5) :1867-1874.
  • 9Nie GJ, Sheftel AD, Kim SF, et al. Overexpression of mitochondrial ferritin causes eytosolic iron depletion and changes cellular iron homeostasis. Blood, 2005. 105 (5) : 2161- 2167.
  • 10Yuan J, Lovejoy DB, Richardson DR. Novel di-2-pyridylderived iron chelators with marked and selective antltumor activity: in vitro and in vivo assessment. Blood, 2004 ; 104(5) : 1450-1458.

引证文献1

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部