Research progress of ferroptosis in the treatment of leukemia / 国际肿瘤学杂志

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.

Kaempferol in reversing drug resistance of chronic myelogenous leukemia K562/ADM cells and its related mechanism / 白血病·淋巴瘤

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.

Kaempferol in reversing drug resistance of chronic myelogenous leukemia K562/ADM cells and its related mechanism / 白血病·淋巴瘤

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.

Effect and mechanism of Solanine on proliferation and apoptosis of Jurkat cells / 中华实用儿科临床杂志

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.

Autophagy and multidrug resistance / 国际肿瘤学杂志

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.

Effects of RNAi targeting CDX2 gene expression on biological characters of human leukemia cells and its relevant mechanisms / 天津医药

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.

Expression and role of HOXC gene in tumor / 国际肿瘤学杂志

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.

Expression and significance of HA117 gene in tumor / 国际肿瘤学杂志

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.

Influence of targeted silence HOXA10 gene on leukemia NB4 cells / 白血病·淋巴瘤

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.

Diagnostic value of N-terminal pro-brain natriuretic peptide and MB isoenzyme of creatine kinase for heart failure in pneumonia children / 临床儿科杂志

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.

Relationship between FOX family genes and leukemia / 国际儿科学杂志

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.

Effects of tetramethylpyrazine injection on the proliferation and apoptosis of Jurkat cells and the relevant molecular mechanisms / 白血病·淋巴瘤

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.

Progress of SF3B1 gene mutation and hematological malignancies / 国际儿科学杂志

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.

Screening and verification of the siRNA targeting Apollon / 白血病·淋巴瘤

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.

Selection and functional identification of siRNA targeting of HOXA7 / 肿瘤研究与临床

Objective To design and screen small interefere RNA (siRNA) targeting of HOXA7,and to investigate the effect of the siRNA on human lung cancer LETP-a-2 cells proliferation and apoptosis in vitro.Methods Three pairs of siRNA targeting of HOXA7 and one pair of siRNA for negative control were transfected respectively into LETP-a-2 cells through cationic liposome.The mRNA and proteion expression levels of HOXA7 were observed by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.The effect of HOXA7 siRNA on growth and apoptosis of LETP-a-2 cells were measured by MTT and flow cytometry.Results All the three pairs of siRNA could inhibit HOXA7 expression effectively,among which siRNA2 got the best effects,the silence rates were (57.344±4.743) ％ on mRNA level and (52.219±0.550) ％ on protein leval.The proliferation was inhibited and the apoptosis was promoted by the siRNA targeting HOXA7 in LETP-a-2 cells,among which siRNA2 got the favourite results,the inhibitory rate was (48.144±4.992) ％ and the apoptosis rate was (26.613±0.612) ％.Conclusion The siRNA2 targeting of HOXA7 enrolls in promoting apoptosis and inhibiting grows of LETP-a-2 cells,indicating that manipulation of HOXA7 expression may be a potential therapeutic strategy for cancer.

Reversion of multidrug resistance in leukemia K562 cells by RNA interference targeting Apollon gene / 中国癌症杂志

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.

FHIT gene and tumor / 国际肿瘤学杂志

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.

Effects of RNA interference targeting HOXA9 on the proliferation and apoptosis of human acute monocytic leukemia U937 cells / 肿瘤研究与临床

Objective To investigate the effects of small interference RNA (siRNA) targeting HOXA9 on the proliferation and apoptosis of human acute monocytic leukemia U937 cell line.Methods Effective and specific siRNA oligo targeting HOXA9 was designed and compounded.It was transfected transiently into U937 cells by cationic liposome.The cells was divided into three groups:experimental group(siRNA targeting HOXA9 was transfected by liposome),negative control group (negative siRNA was transfected by liposome) and cell control group (add equal cells and medium).The expression of HOXA9 mRNA and protein were detected by reverse transcription PCR and Western blot.The cell proliferation was assessed by MTT.The apoptosis of each group were measured by Annexin V-FITC.Results Aftcr transfected by siRNA targeting HOXA9,the relative mRNA expression levels of HOXA9 in the experimental group,negative control group and cell control group were (22.980±0.548) ％,(82.371±1.517) ％ and (84.637±2.252) ％,respectively (P ＜ 0.05),and the relative protein expression levels were (50.377±2.773).％,(105.500±3.900) ％ and (111.392±3.905) ％,respectively (P ＜ 0.05).The inhibitory rates of cell proliferation and the apoptosis rates of the experimental group were significantly increased.The inhibitory rates of cell proliferation of 24 h,48 h and 72 h were (41.909±4.333) ％,(54.470±3.756) ％ and (65.835±1.024) ％,respectively,and the apoatosis rate was (26.800±2.081) ％.Compared with 2 controls,the experimental group differences had statistically significance (P ＜ 0.05).Conclusion siRNA targeting HOXA9 can effectively silence HOXA9 gene expression in U937 cell,suppress cell proliferation and induce cell apoptosis obviously,which providing experimental basis for clinical lenkemia therapy by targeting HOXA9 gene.

CDX gene and tumor / 国际肿瘤学杂志

The caudal-type homeobox gene is a member of homeobox gene—Para-HOX family,including CDX1,CDX2 and CDX4.As a transcriptional factor,CDX plays an important role in embryo development,hematopoietic system formation,intestinal epithelium tissue development and so forth.The abnormal expression of CDX is usually closely related with tumorigenesis.Researching the relationship between CDX and tumors will contribute to tumor diagnosis and treatment.

Progress of homeobox gene family in nervous system / 国际儿科学杂志

Homeobox gene family encode a kind of transcription regulatory factors,which can specifically combine and regulate target genes,control embryonic development,cell proliferation and differentiation.Several subfamilies of homeobox gene famiy are associated with the early stage of differentiation and development of nervous system,whose abnormal expression explain the occurrence and development of nervous system diseases.Further study between homeobox gene family and nervous system can help to prevent and treat that diseases.