Journal of Jilin University Medicine Edition ›› 2017, Vol. 43 ›› Issue (05): 937-942.doi: 10.13481/j.1671-587x.20170515

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Influence of autophagy inhibited by chloroquine in apoptosisof myelogenous leukemia cells promoted by decitabine

XING Lina, REN Jinhai, WANG Ying, WANG Fuxu, CAI Shengxin   

  1. Department of Hematology, Second Hospital, Hebei Medical University, Shijiazhuang 053600, China
  • Received:2017-02-07 Online:2017-09-28 Published:2017-09-29

Abstract: Objective: To study the influence of chloroquine combined with decitabine in the apoptosis of leukemia K562 cells and KG-1a1Aor1a cells, to explore the effect of autophagy on the leukemia cell apoptosis induced by decitabine, and to clarify its mechanism. Methods: The leukemia K562 and KG-1a1Aor1a cells were cultivated in vitro and divided into blank control group, decitabine group (10 μmol·L-1) and chloroquine(50 μmol·L-1) combined with decitabine group (combined group). The leukemia cells in combined group were pre-treated with chloroquine for 6 h before experiment. After treatment with drugs for 24 and 48 h, the number of cells was detected and by CCK-8 method the inhibitory rates of proliferation cells were calculated;the apoptotic rates and mitochondrial membrane potential were detected by flow cytometry. Q-PCR method was carried out to determine the gene expression levels of Atg7 and Atg12, and Western blotting was used to test the protein expression of LC3. Results: After treatment for 24 and 48 h, the number of K562 and KG-1a1Aor1a cells in decitabine group and combined group were decreased compared with blank control group(P<0.05 or P<0.01); the apoptotic rates and mitochondrial membrane potential were remarkably increased (P<0.05 or P<0.01). Compared with decitabine group, the number of K562 and KG-1a1Aor1a in combined group was significantly decreased, and the apoptotic rates were remarkably increased (P<0.05). After treatment for 24 h, the expression levels of Atg7, Atg12 and LC3-Ⅱ/LC3-Ⅰ in the leukemia K562 and KG-1a1Aor1a cells in decitabine group were significantly increased compared with blank control group (P<0.05 or P<0.01);the expression levels of Atg7, Atg12 and LC3-Ⅱ/LC3-Ⅰ in the leukemia K562 and KG-1a1Aor1a cells in combined group were significantly decreased compared with decitabine group (P<0.05 or P<0.01). Conclusion: Decitabine could promote the apoptosis of leukemia cells, and the inhibition of autophagy by chloroquine can promote the apoptosis induced by decitabine.

Key words: decitabine, chloroquine, autophagy, apoptosis

CLC Number: 

  • R733.7