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Transforming growth factor-β (TGF-β) /Smad signaling pathway is an important signaling pathway in human cells, which can regulate life activities such as cell growth, proliferation and apoptosis, and its signal transduction consists of ligand and receptor binding, intracytoplasmic signaling pathway, as well as interactions within the cell nucleus. This signaling pathway is closely related to the pathogenesis, drug resistance, recurrence and prognosis of acute leukemia. Exploring the potential of direct inhibitors, related therapeutic targets and natural extracts of this signaling pathway for the treatment of leukemia can provide new ideas for the study of biomarkers and targeted gene therapy for leukemia.
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Pyroptosis is a programmed cell death mediated by the Gasdermin family of proteins, which is different from apoptosis and necrosis and accompanied by the release of a large number of pro-inflammatory factors. Leukemia is a malignant proliferative disease derived from hematopoietic stem cells, the pathogenesis and progression of which are related to many factors. In recent years, with the in-depth study on the mechanism of pyroptosis, it has been found that pyroptosis is closely related to the occurrence and development of leukemia. Further study of the mechanism of pyroptosis in leukemia can provide a new idea for the diagnosis and treatment of leukemia.
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Objective To investigate the mechanism of luteolin's(Lut)reversal effect on multidrug resistance of chronic myeloid leukemia K562/ADR cells.Methods CCK-8 assay was used to detect drug resistance in K562 and K562/ADR cells 24 hours after treatment with different doses of adriamycin(ADR).CCK-8 assay was used to assess the cytotoxicity and sensitizing effect of Lut on ADR after K562/ADR cells were treated with Lut alone or in combination with ADR for 24 hours.K562/ADR cells in logarithmic growth phase were separated into three group:0μmol/L Lut,2μmol/L and 4μmol/L Lut groups.ADR accumulation in cells was measured using flow cytometry.Nuclear factor erythroid-2-related factor 2(Nrf2),multidrug resistance associated protein 1(MRP1),P-glycoprotein(P-gp)and glutathione-S-transferase-PI(GST-pi)mRNA and protein expressions were identified using RT-PCR and Western blot assay.Glutathione(GSH)kit was used to detect intracellular GSH content.Results Compared with K562 cells,K562/ADR cell line was significantly resistant to ADR,and the drug resistance was 53.69 times.K562/ADR cell proliferation was decreased to variable degrees by different doses of Lut when compared to the 0μmol/L Lut group(P＜0.05).The proliferation inhibition rates of K562/ADR cells treated with 2 and 4μmol/L Lut were less than 10%,indicating that the concentration of Lut was non-toxic.Compared with the 0 μmol/L Lut group,the 2 μmol/L Lut group and the 4 μmol/L Lut group showed significantly increased ADR growth inhibition rate on K562/ADR and increased accumulation of ADR in cells,improved the reversal resistance fold,and decreased GSH content in cells.MRP1,P-gp,GST-pi and Nrf2 mRNA and protein expression were reduced in cells(P＜0.05).The effect of 4 mol/L Lut was greater than that of 2 mol/L Lut.Conclusion Lut may decrease K562/ADR cell proliferation and reverse ADR medication resistance.The mechanism could be connected to the downregulation of Nrf2,MRP1,P-gp and GST-pi expression,which leads to an increase in ADR accumulation in K562/ADR cells.
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Objective:To investigate the effect of luteolin(Lut)on the proliferation and ferroptosis of human adriamycin(ADR)resistant chronic myeloid leukemia(CML)K562/ADR cells and the underlying molecular mechanism. Methods:K562 and K562/ADR cells were treated with different concentrations of ADR.The sensitivity of K562 and K562/ADR cells to ADR was evaluated by CCK-8 assay;the effect of different concentrations of Lut on the proliferation of K562/ADR cells was assessed by CCK-8 assay,and the half inhibitory concentration(IC50)was calculated for subsequent experiments;the morphological changes of the cells were observed by an inverted microscope;CCK-8 assay was used to examine the sensitizing effect of Lut on ADR;FCM assay was used to study the effect of Lut on the apoptosis of K562/ADR cells;fluorescence probe DCFH-DA,Fe2+colorimetric assay and glutathione(GSH)kit were used to detect the content of reactive oxygen species(ROS),Fe2+and GSH in K562/ADR cells,respectively;Western blotting was used to examine the expression levels of glutathione peroxidase 4(GPX4),nuclear factor erythroid 2-related factor 2(Nrf2)and heme oxygenase-1(HO-1)in K562/ADR cells;the effects of Lut on the proliferation of K562/ADR cells,ROS content,GSH content,Fe2+content and GPX4 expression were studied after treatment with ferroptosis inhibitor Ferrostatin-1(Fer-1). Results:Compared with control group(cells treated with 0 μmol/L Lut),Lut significantly inhibited the proliferation of K562/ADR cells(P＜0.001),improved the chemosensitivity of K562/ADR cells to ADR(P＜0.05),increased apoptosis rate(P＜0.001)and ROS level(P＜0.05)of K562/ADR cells,reduced the GSH level(P＜0.001),and increase Fe2+content(P＜0.01).Compared with control group(cells treated with 0 μmol/L Lut),the protein expressions of GPX4,Nrf2 and HO-1 decreased with the increase of Lut concentration(P＜0.05).Compared with the Lut treatment alone,the inhibitory effect on the proliferation of K562/ADR cells induced by Lut was partially restored by Fer-1 intervention(P＜0.05),and intracellular ROS level was decreased(P＜0.001),GSH level was increased(P＜0.001),Fe2+content was decreased(P＜0.001)and the expression of GPX4 was increased(P＜0.01)in K562/ADR cells. Conclusion:Lut can inhibit the proliferation of K562/ADR cells through ferroptosis pathway,improve the chemosensitivity to ADR,and the potential mechanism may be related to the Nrf2/HO-1 signaling pathway,which provides experimental basis for the treatment of leukemia by ferroptosis.
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Leukemia is a group of hematologic malignancie. Ferroptosis is a novel of cell death caused by iron-dependent lipid peroxidation accumulation, which participates in the occurrence and development of leukemia. Activation of different regulatory sites in the ferroptosis pathway can promote the death of leukemia cells. Therefore, it can provide a new direction for the treatment of leukemia by inducing ferroptosis of cells.
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Objective@#To investigate the drug resistance of kaempferol reversed adriamycin (ADM)-resistant K562/ADM cells in chronic myelogenous leukemia (CML) and its related mechanism.@*Methods@#Methyl thiazolyl tetrazolium (MTT) method was used to detect the toxicity of ADM on K562 and K562/ADM cells for 24 h. The half inhibitory concentration (IC50) of ADM and the drug resistance multiple for 24 h were calculated. MTT method was used to detect the toxicity of kaempferol on K562/ADM cells for 24 h. The 5% inhibitory concentration (IC5) and 10% inhibitory concentration (IC10) of kaempferol for 24 h were calculated to determine the concentration of kaempferol in the subsequent experiments. And the cells untreated by the kaempferol were selected as the control group. The cell inhibition after the treatment of ADM for 24 h of the blank control group and kaempferol intervention group was detected by using MTT method. And then the cell inhibition for 24 h and ADM IC50 for 24 h in the above groups were calculated. The ratio of IC50 in the blank control group and kaempferol group was the reversal drug resistance multiple of kaempferol. The fluorescence intensity of ADM in K562/ADM cells treated by kaempferol was detected by using flow cytometry. Western blotting was used to detect the expressions of P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1), phosphorylated p38 (p-p38), and total p38 (t-p38) protein in K562/ADM cells after the treatment of kaempferol, the specific inhibitor of p38-MAPK signaling pathway SB202190, and the combination of kaempferol and SB202190.@*Results@#After the treatment of ADM for 24 h, the IC50 value of K562 and K562/ADM cells was (0.9±0.6), (28.1 ±3.5) μg/ml, respectively. The drug resistance multiple of K562/ADM cells on the treatment of ADM for 24 h was 31.16 compared with the K562 cells. MTT method showed that kaempferol inhibited the proliferation of K562/ADM cells in a dose-dependent manner. According to the IC5 and IC10, 0.5 μmol/L and 1.0 μmol/L kaempferol were determined to do the subsequent experiments. After the combined interaction of kaempferol and ADM for 24 h, the ADM IC50 of K562/ADM cells in the blank control group, 0.5 μmol/L kaempferol group and 1.0 μmol/L kaempferol group was (33.7±5.7), (21.4±0.6), (15.9±1.8) μg/ml, respectively (F = 30.85, P < 0.05), and there was a statistical difference of pairwise comparison (both P < 0.05). The reversal drug resistance multiple of K562/ADM cells for 24 h in 0.5 μmol/L kaempferol group and 1.0 μmol/L kaempferol group was 1.58 and 2.12, respectively. Flow cytometry results showed that the mean fluorescence intensity (MFI) of ADM in the blank control group, 0.5 μmol/L kaempferol group and 1.0 μmol/L kaempferol group was 138.4±8.9, 154.3±2.2, 165.7±4.8, respectively, and the difference was statistically significant (F = 161.48, P < 0.05). Compared with the blank control group, after treatment of K562/ADM cells with 0.5 μmol/L and 1.0 μmol/L kaempferol for 24 h, the relative expressions of P-gp, MRP1 and p-p38 protein were decreased in K562/ADM cells (all P < 0.05), but there was no statistical difference in the expression of t-p38 protein (P > 0.05); SB202190 could reduce the relative expressions of P-gp, MRP1 and p-p38 protein (all P < 0.05); after the treatment of SB202190 combined with different concentration of kaempferol, the relative expressions of P-gp, MRP1 and p-p38 protein in K562/ADM cells did not decrease (P > 0.05).@*Conclusions@#Kaempferol can decrease the relative expressions of P-gp and MRP1 in K562/ADM cells by inhibiting p38-MAPK pathway, so as to increase the concentrations of ADM and to reverse the drug resistance of K562/ADM cells.
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Objective:To investigate the drug resistance of kaempferol reversed adriamycin (ADM)-resistant K562/ADM cells in chronic myelogenous leukemia (CML) and its related mechanism.Methods:Methyl thiazolyl tetrazolium (MTT) method was used to detect the toxicity of ADM on K562 and K562/ADM cells for 24 h. The half inhibitory concentration ( IC50) of ADM and the drug resistance multiple for 24 h were calculated. MTT method was used to detect the toxicity of kaempferol on K562/ADM cells for 24 h. The 5% inhibitory concentration ( IC5) and 10% inhibitory concentration ( IC10) of kaempferol for 24 h were calculated to determine the concentration of kaempferol in the subsequent experiments. And the cells untreated by the kaempferol were selected as the control group. The cell inhibition after the treatment of ADM for 24 h of the blank control group and kaempferol intervention group was detected by using MTT method. And then the cell inhibition for 24 h and ADM IC50 for 24 h in the above groups were calculated. The ratio of IC50 in the blank control group and kaempferol group was the reversal drug resistance multiple of kaempferol. The fluorescence intensity of ADM in K562/ADM cells treated by kaempferol was detected by using flow cytometry. Western blotting was used to detect the expressions of P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1), phosphorylated p38 (p-p38), and total p38 (t-p38) protein in K562/ADM cells after the treatment of kaempferol, the specific inhibitor of p38-MAPK signaling pathway SB202190, and the combination of kaempferol and SB202190. Results:After the treatment of ADM for 24 h, the IC50 value of K562 and K562/ADM cells was (0.9±0.6), (28.1 ±3.5) μg/ml, respectively. The drug resistance multiple of K562/ADM cells on the treatment of ADM for 24 h was 31.16 compared with the K562 cells. MTT method showed that kaempferol inhibited the proliferation of K562/ADM cells in a dose-dependent manner. According to the IC5 and IC10, 0.5 μmol/L and 1.0 μmol/L kaempferol were determined to do the subsequent experiments. After the combined interaction of kaempferol and ADM for 24 h, the ADM IC50 of K562/ADM cells in the blank control group, 0.5 μmol/L kaempferol group and 1.0 μmol/L kaempferol group was (33.7±5.7), (21.4±0.6), (15.9±1.8) μg/ml, respectively ( F = 30.85, P < 0.05), and there was a statistical difference of pairwise comparison (both P < 0.05). The reversal drug resistance multiple of K562/ADM cells for 24 h in 0.5 μmol/L kaempferol group and 1.0 μmol/L kaempferol group was 1.58 and 2.12, respectively. Flow cytometry results showed that the mean fluorescence intensity (MFI) of ADM in the blank control group, 0.5 μmol/L kaempferol group and 1.0 μmol/L kaempferol group was 138.4±8.9, 154.3±2.2, 165.7±4.8, respectively, and the difference was statistically significant ( F = 161.48, P < 0.05). Compared with the blank control group, after treatment of K562/ADM cells with 0.5 μmol/L and 1.0 μmol/L kaempferol for 24 h, the relative expressions of P-gp, MRP1 and p-p38 protein were decreased in K562/ADM cells (all P < 0.05), but there was no statistical difference in the expression of t-p38 protein ( P > 0.05); SB202190 could reduce the relative expressions of P-gp, MRP1 and p-p38 protein (all P < 0.05); after the treatment of SB202190 combined with different concentration of kaempferol, the relative expressions of P-gp, MRP1 and p-p38 protein in K562/ADM cells did not decrease ( P > 0.05). Conclusions:Kaempferol can decrease the relative expressions of P-gp and MRP1 in K562/ADM cells by inhibiting p38-MAPK pathway, so as to increase the concentrations of ADM and to reverse the drug resistance of K562/ADM cells.
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Objective To explore the effect of proliferation and apoptosis of Solanine on acute T lymphocyte leukemia (T-ALL) Jurkat cells and its mechanism.Methods After treated with different concentrations of Solanine,the proliferation of Jurkat cells was detected by CCK-8 assay,and the effect of Solanine on apoptosis of Jurkat cells were detected by flow cytometry.The expression of Bcl-2 and Bax in Jurkat cells were detected by Western blot,and the expression levels of Bcl-2 mRNA and Bax mRNA were detected by real-time fluorescence quantitative polymerase chain reaction.Results CCK-8 assay showed that Solanine significantly inhibited the proliferation of Jurkat cells in a dose-and time-dependent manner.The results of flow cytometry showed that the apoptosis rates of Jurkat cells treated with Solanine for 24 h were (2.40-± 0.98) ％,(28.43-± 4.86) ％,(41.56-± 1.87) ％,respectively,in a dose-dependent manner.Western blot showed that Solanine could increase the expression of Bax and decrease the expression of Bcl-2 in Jurkat cells,and they all were dose-dependent.Conclusion Solanine can significantly inhibit the proliferation and induce apoptosis of Jurkat cells.The mechanism is related to the up-regulation of Bax expression and down-regulation of Bcl-2 expression.
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Multidrug resistance (MDR) is the main reason for the failure of leukemia chemotherapy.Autophagy plays an important role in the regulation of MDR.On one hand,as a mechanism of programmed cell death,autophagy can directly induce the death of MDR cells.On the other hand,protective autophagy induced by different signaling pathways and factors such as Hedgehog (Hh) signaling pathway and p53 can promote the survival of MDR cells.Therefore,autophagy agonist or autophagy inhibitors combined with chemotherapeutics will be a new strategy for the treatment of leukemia.
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As a member of homeobox gene family,HOXC is expressed in many organs and can regulate gene expression,cell differentiation and morphogenesis.Abnormality of its function is closely related to the prognosis of leukemia,breast cancer,renal cell carcinoma,prostate cancer and so on.
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Objective To detect the effects of siRNA targeting CDX2 gene expression on of BCR-ABL, caspase and Bax expressions, and the mechanisms thereof. Methods According to the earlier experiments, siRNA specifically targeting CDX2 gene (CDX2-siRNA) and the negative control sequence (CDX2-siRNA-NC) were selected, and then were transfected into K562 cells by Roche X-tremeGENE HP DNA Transfection Reagent. The flow cytometry analysis was used to detect the effects of siRNA on cell apoptosis. The expressions of BCR-ABL, caspase-9, Bax mRNA and protein were tested by RT-PCR and Western blot assay. Results MTT and flow cytometry analysis showed that after the silence of CDX2 gene expression, the proliferation of K562 cells was prohibited and the apoptotic rate of K562 cells was distinctly increased compared with that of normal cell group, but the negative control group had no significant change. According to the RT-PCR and Western blot assay, in comparison with the normal cell group and the negative control group, the expression levels of BCR-ABL mRNA and protein were obviously decreased, and the difference was statistic significance. On the other hand, the expressions of caspase-9 and Bax mRNA and protein were significantly higher than those of other two groups (P<0.05). Conclusion CDX2-siRNA can promote apoptosis of K562 cells obviously, and the mechanism is related with the down-regulation of BCR-ABL and the up-regulation of caspase-9 and Bax.
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FOX genes code transcription factors. FOXO3a,FOXM1,FOXP3 are members of FOX genes family,which are associated with leukemia. Phosphorylated FOXO3a which loses the function of suppressing leu-kemia is inactive. Phosphorylated FOXO3a expresses in leukemic cell cytoplasm. FOXM1 is an oncogenesis tran-scription factor. FOXM1 highly expresses in myeloid leukemic cells. Expression of FOXP3 in leukemic cells has diversity. FOXP3 mainly expresses in T cell leukemic cells. These genes abrrant expressions play a key role in leukemia pathogenesis,development,therapy,drug resistance and prognosis.
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HA1 1 7,as a multiple drug resistance(MDR)gene,has recently been discovered.It may mediate the MDR of tumor through Bcl-2 anti-apoptotic pathways.HA1 1 7 gene exists high expression in leuke-mia,lymphoma,breast cancer,neuroblastoma,colon adenocarcinoma and so on,and its overexpression is closely associated with the MDR and poor prognosis of these tumors.
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Objective To explore the effects of lentivirus-mediated RNA interference targeting HOXA10 gene on the proliferation, apoptosis and drug resistance of leukemic cell line NB4.Methods NB4 cells were divided into three groups: interference group, negative control group and untreated group.The infection efficiency of lentivirus for NB4 cells was detected by flow cytometry, and the expression of HOXA10 gene of NB4 cells at mRNA and protein level was detected by real-time PCR and Western blot.Cell survival was determined by MTF assay, and apoptosis and necrosis rates were detected by flow cytometry.Western blot was used to detect the influence of down-regulation HOXA10 gene on the multi-drug resistance-1 (MDR-1) protein.Results The ratio of GFP positive cells was up to 90 ％.HOXA10 gene mRNA and protein levels were decreased in interference group compared with control group.The inhibition rate of interference group was (52.12±4.02) ％, the apoptosis rate of interference group was (30.0±2.7) ％, and their differences in the interference group and in control groups (negative control group and untreated group) were significant (P ＜ 0.05).Western blot results showed that interfering HOXA10 gene significantly reduced the resistance gene MDR-1 expression level and reverse the drug-resistant of leukemia cells.Conclusions Lentivirns-shHOXA10 can steadily reduce the expression level of HOXA10, inhibit the leukemic cells proliferation, promote apoptosis and reverse drug-resistant.HOXA10 gene is expected to become a new target for reversing leukemia drug resistance.
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Objective To study the effect of tetramethylpyrazine injection on proliferation and apoptosis of human acute lymphoblastic leukemia (ALL) cell line Jurkat and the relevant molecular mechanisms.Methods Cells were treated with tetramethylpyrazine injection at various concentrations (0,0.25,0.50,0.75,1.00,1.25 and 1.50 mg/ml),CCK-8 method was used to detect the inhibition rates at 24,48 and 72 h.After cells were treated with different concentrations of tetramethylpyrazine injection (0,0.50,1.00 and 1.50 mg/ml) for 48 h,the cell cycle and apoptosis were detected by flow cytometry,and the Aurora-B and Survivin protein expression were analyzed by Western blot.Results Compared with the control group (cells without tetramethylpyrazine injection treatment),various concentrations of tetramethylpyrazine injection could effectively inhibit Jurkat cells proliferation in a time-and dose-dependent manner (P ＜ 0.05),and IC50 at 24 h,48 h and 72 h after treatment were (1.33±0.16),(0.91±0.10) and (0.67±0.11) mg/ml,respectively.After cells were treated with tetramethylpyrazine injection at different concentrations (0.5,1.0 and 1.5 mg/ml) for 48 h,the number of treated cells in G2/M phase was increased,but that in S phase was decreased,and the apoptosis rates were significantly higher than that of control group,with a dose dependence (P ＜ 0.05).The results of Western blot showed that the expression levels of Aurora-B and Survivin in treated cells were lower than that of control group,also with a dose dependence (P ＜ 0.05).Conclusions Tetramethylpyrazine injection can effectively inhibit proliferation and induce apoptosis of Jurkat cells in vitro,and its underlying mechanisms involve with down-regulation of the Aurora-B and Survivin protein expression.
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ObjectiveTo investigate the diagnostic value of N-terminal pro-brain natriuretic peptide (NT-proBNP) and MB isoenzyme of creatine kinase (CK-MB) for heart failure (HF) in pneumonia children.MethodsThe NT-proBNP and CK-MB were assayed in 132 pneumonia children with HF, 138 pneumonia children without HF and 62 healthy children were recruited into this study. A receiver operating characteristics (ROC) curve and a logistic regression model were employed to assess the diagnostic accuracy of NT-proBNP and CK-MB for HF in pneumonia children.ResultsPneumonia children with HF had higher blood NT-proBNP and CK-MB than those in pneumonia children without HF and healthy controls (P<0.01 for both). Pneumonia children with HF had higher blood NT-proBNP and CK-MB than the pneumonia children without HF. The area under curves (AUCs) of NT-proBNP and CK-MB for HF were 0.85 and 0.72, respectively. The AUC for their combinational usage was 0.87.ConclusionBoth NT-proBNP and CK-MB are effective markers as diagnostic adjuncts for HF in pneumonia children. Combination of NT-proBNP and CK-MB can improve the diagnostic accuracy for HF in pneumonia children.
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The SF3B1 gene encodes subunit 1 of the splicing factor 3b,which is a core component of the U2 small nuclear ribonucleoprotein and plays an important role in the process of RNA splicing. Abnormal splicing caused by SF3B1 mutations are associated with hematological malignancies,particularly with myelodys-plastic syndrome,refractory anemia with ring sideroblasts associated with marked thrombocytosis and chronic lymphocytic leukemia( CLL) . In myelodysplastic syndrome and refractory anemia with ring sideroblasts associat-ed with marked thrombocytosis,SF3B1 mutations are bond up with favorable prognosis and strongly with ring sideroblasts. But in CLL,SF3B1 mutations are factors of poor prognosis.
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Objective To screen siRNAs that can effectively inhibit Apollon gene expression and determine the cellular functions of those siRNAs.Methods A chemical synthesis method was used to synthesize 3 siRNA sequences against different sites of Apollon.They were transfected into the human breast cancer MCF-7 cells by using Lipofectamine 2000.mRNA level of Apollon was determined by reverse transcription-polymerase chain reaction (RT-PCR).Cellular immunity fluorescence quantitative analysis combined with confocal laser technology was used to determine the protein level of Apollon.Methyl thiazolyl tetrazolium bromide (MTT) assay and flow cytometry were used to determine the effects of siRNA targeting Apollon on proliferation and apoptosis of MCF-7 cells,respectively.Results Three pairs of siRNA could significantly inhibit Apollon mRNA expression,at the inhibition rates of (36.201±11.629) ％,(67.308±7.686) ％and (47.123±12.000) ％,respectively (P ＜ 0.05).After tranfection by siRNA2,Apollon protein fluorescence intensity was (14.97±2.08) ％ compared with control cells.The cell proliferation MCF-7 was inhibited by (73.361±2.118) ％and apoptosis was increased by (28.793±0.743) ％.Conclusions Screened siRNA2 effectively silences Apollon gene expression,effectively inhibits the proliferation and increases the apoptosis of MCF-7 cells.This provids the foundation for its clinical application in cancer therapy.
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The human fragile histidine triad (FHIT) gene is a tumor suppressor gene,which is located at chromosome region 3p14.2.The fragile site FRA3B of the FHIT gene is the most unstable site.FHIT can promote apoptosis,and inhibit cell proliferation and tumorigenesis.High methylation status,loss of the various sections of the FHIT gene,changes of the fragile site FRA3B and abnormalities of FHIT transcripts can result in gene afunction,and then promote the development and progression of various types of cancers.Transfecting wild-type FHIT into tumor cells with low or lacking endogenous FHIT expression can induce apoptosis.The combined treatment with other genes may provide a new insight for the treatment of tumors.
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Background and purpose:Apollon gene is highly expressed in leukemia and other tumors. The study aimed to discuss whether RNAi technology can reverse multidrug resistance of chronic myeloid leukemia cell line K562 through constructing a eukaryotic vector of short hairpin RNA (shRNA) targeting at Apollon gene. Methods:The eukaryotic vector pGPHI-GFP-Neo-Apollon with shRNA targeting at Apollon gene was constructed and then transfected into K562 cells by LipofectamineTM2000, and G418 pressure selection. Reverse transcription-polymerase chain reaction (RT-PCR) and immunolfuorescence were used to detect the expression of Apollon mRNA and protein after Apollon was transfected stably in K562 cells. The changes of sensitivity of K562 cells to leurocristine (VCR) and etoposide (VP16) after transfection with shRNA-Apollon were detected by MTT method, and the apoptosis rate was detected by flow cytometry. Results: pGPHI-GFP-Neo-Apollon carrier was constructed successfully and expressed stably in K562 cells, and after G418 screening, it silenced Apollon mRNA and protein expression effectively. According to the result of MTT, the sensitivity of K562 cells to VCR and VP16 increased significantly in the group of gene interference, with half of its inhibition concentration (half-inhibitory, IC50) value signiifcantly lower than the control group (P0.05). Conclusion:pGPHI-GFP-Neo-Apollon carrier can enhance the abilities of VCR and VP16 to induce the apoptosis of K562 cells, namely an increase of sensitivity to these chemotherapeutics in K562 cells, it is hinted that RNA interference targeting Apollon gene may reverse the multidrug resistance of leukemia cells in some degree.