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  • Ding, Jia-Hua  (23)
  • 2005-2009  (23)
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  • 2005-2009  (23)
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  • 1
    Online Resource
    Online Resource
    Synergistic Effect of Magnetic Nanopartical Fe304, Au and Daunomycin on K562/A02.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4171-4171
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4171-4171
    Abstract: Objective: This paper was to study the reversal effect of magnetic Nano-Fe3O4 or Nano-Au with DNR, on multidrug resistance cell line K562/A02 and to investigate the reversal mechanism of this combination, and to provide theoretic evidence for the clinical application of them as resistance modifying agents. Method: The IC50 (the concentration causing 50% inhibition of cell growth) of DNR, Nano-Fe3O4 and Nano-Au respectively were assayed by MTT method.The drug-loaded nanoparticles were prepared by solvent diffusion method.Some nanoparticales, volume ratio from 1.5% to 50%, were combined with some DNR to find the best combination to prepare best drug-loaded nanopartilces.At last, the K562/A02 cells was treated with the composite of 25% nanoparticales and 10mg/L DNR, which MDR1 mRNA was assayed by RT-PCR;intracellular drug concentration and the apoptosis was determined by fluorometry and confocal fluorescence microscope. Results: The IC50 of DNR for K562/A02 and K562 cells were 23.23mg/L and0.307mg/L respectively.Two nanoparticles themselves have not evident cytotoxic effect to K562/A02 and K562 cells.Pretreating K562/A02 cells with the composite of 25% nanoparticales and 10mg/L DNR for 48 hours partially restored the sensitivity of K562/A02 cells to DNR;K562/A02 showed apoptotic characteristics after treated with this composite;drug-loaded nanopartilces elevated the intracellular DNR accumulation in K562/A02 and its MDR1 mRNA were down regulated.Data was analyzed by SPSS 11.5 software and expressed as mean ± SD. Conclusions: Nano- Fe3O4 or Nano-Au can increases the intracellular free DNR concentration of the K562/A02 cells, which lead to more K562/A02 cells apoptosis. Two nanoparticles themselves could not lower the MDR1 gene expression of the K562/A02 cells, but they degraded the MDR1 gene level with combine DNR. These results suggested that Nano- Fe3O4 or Nano-Au with DNR can reverse the resistance of K562/A02 cells significantly.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4171.4171
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
    Online Resource
    Online Resource
    Platelet-Derived Microparticles Induce Angiogenesis In Vitro and In Vivo.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 3901-3901
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 3901-3901
    Abstract: Objective: An attempt was made to investigate the effect of platelet-derived microparticles (PMPs) on the angiogenesis. Methods: Thrombin was adopted to activate the platelets to release PMPs. Flow cytometry(FCM)was adopted to evaluate the efficiencies of different concentrations of thrombin to produce PMPs and BCA was adopted to evaluate the content of PMPs. By the carrier of human umbilical vein cell line ECV-304 cultivated in vitro, investigate the effect of PMPs on the proliferation and apoptosis of human umbilical vein endothelial cells using MTT and FCM. PMPs were put into CAM and observe the effects of PMPs on angiogenesis in Chick embryo chorioallantoic membrane (CAM). Results: The efficiencies of PMPs activated by 1.0U/ml thrombin were 50.1%; PMPs induced proliferation of human umbilical vein cell line ECV-304 in a dose dependent manner. At the concentration of 40ug/ml PMPs, the proliferation rate of human umbilical vein cell line ECV-304 was as 1.8±0.3 times as control and there was no difference with the group of vascular endothelial growth factor (VEGF),which the proliferation rate was 1.9±0.5 times vs. control, p & gt; 0.05;PMPs inhibited human umbilical vein cell line ECV-304 apoptosis. Compared with control group (apoptosis rate 9.4%±0.5%), apoptosis rate of PMPs (40μg/ml) is 3.9%±0.4%, which was significantly reduced, p & lt;0.05. The addition of VEGF (10μl/ml) did not successfully prevented apoptosis of human umbilical vein cell line ECV-304 (apoptosis rate 8.0%±0.8%);After 72 h of incubation, showing an implant of PMPs by allantoic vessels developing radially towards it (implant) in a ’spoked-wheel’ pattern, at the concentration of 80μg/ml PMPs, number of vessel ramification is 112.5±11.31 and vessel area/CAM area is (6.19±1.29)%, compared with the VEGF(p & gt;0.05). But there are not localized allantoic vessels developing in the NS control group(P & lt;0.05). Conclusion: 1.0U/ml thrombin activated platelet could get the best efficiency of PMPs, which could stimulate proliferation of human umbilical vein cell line ECV-304 and inhibit its apoptosis and PMPs have certain promotive effect on the formation of capillary in chick chorioallantoic membranes.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.3901.3901
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
    Online Resource
    Online Resource
    Reversal of P-Glycoprotein-Dependent Resistance to Adriamycin by 5-bromotetrandrine in K562/A02 Cell Line.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4175-4175
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4175-4175
    Abstract: Objective: The present study aimed to evaluate the MDR reversal activity of bromotetrandrine (BrTet), a bromized derivative of tetrandrine (Tet), in vitro. Methods: Drug sensitivity was determined using the MTT assay. Adriamycin (ADM) accumulation, the protein levels of P-glycoprotein (P-gp) and the apoptotic changes were analyzed by fluorospectrophotometry, respectively. The mRNA levels of P-gp was determined by RT-PCR. Results: BrTet at 0.25, 0.5 and reversed ADM resistance in MDR K562/A02 cells dose-dependently and its potency was greater than that of Tet at the same concentrations. The IC50 of ADM for K562 and K562/A02 cells were 55.122 mg/l and 1.1373 mg/l, respectively. Treating K562/A02 cells with BrTet(1uM)and TTD(1uM)both for 48 hours partially restored the sensitivity of K562/A02 cells to ADM (IC50 were 4.7729 mg/l and 13.584 mg/l respectively) but had not effect on K562 cells. The fold reversal (FR) were 11.55 and 4.06 respectively. K562/A02 cells showed apoptotic characteristics after treated with Brtet and Tet both for 48 hours compared with control group(apoptosis rate was 61.1%, 11.1% and 9.9%,respectively); Fluorospectrophotometric assay showed that BrTet significantly increased the intracellular accumulation of ADM in K562/A02 cells in a dose-dependent manner. The fluorescence intensity of intracellelar ADM in K562/A02 cells treated with ADM(1mg/L)was 33% of that in K562 cells. BrTet and Tet elevated the intracellular ADM concentration in K562/A02 cells up to 52% and 69%,respectively. BrTet also inhibited the overexpression of P-gp in K562/A02 cells. The fluorescence intensity of P-gp in K562 and K562/A02 cells was 0.5 and 97.97.The P-gp expression was down after treated with BrTet and TTD (65.05 and 54.86). The mdr1 mRNA was also down regulated. Conclusions: BrTet showed significant MDR reversal activity in vitro. Its activity may be related to the inhibition of P-gp overexpression and the increase in intracellular accumulation of anticancer drugs. BrTet may be a promising MDR modulator for eventual assessment in the clinic.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4175.4175
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
    Online Resource
    Online Resource
    The Effect of Phenylhexyl Isothiocyanate on Drug Resistance of K562/A02 Cell Line
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5061-5061
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5061-5061
    Abstract: Objective: To investigate the effect of 6-phenylhexyl isothiocyanate (PHI) on drug resistance and sensitivity on K562/A02 cell line to ADM and elucidate the probable mechanisms. Methods: We measured growth inhibition of ADM on K562/A02 cell line by MTT assay. Apoptosis rate of K562/A02 cell line, the change of intracellular ADM and MRP1 protein level were detected by Flow Cytometry. Intracellular deoxidized GSH by spectrometric enzyme assay and MRP1 mRNA by RT-PCR semiquantitative assay were observed anteroposterior using PHI. Results: PHI can enhance the sensitivity of K562/A02 cell line to ADM, survival rate of K562/A02 cell line decreased with the increasing concentration of PHI and ADM. Apoptosis rate increased with treating by combination of two above drugs, and multiple of drug resistance had statistical significance (P & lt;0.05) when the concentration of PHI was more than 20μmol/l. Intracellular GSH of K562/A02 cell line reduced 5% when 1μg/ml ADM was single used, and when more than 10μmol/l PHI was used it increased slightly at first then decreased. When more than 20μmol/l PHI and 1μg/ml ADM were used combination, intracellular GSH of K562/A02 cell line decreased progressively with increasing the concentration of PHI. Protein and gene level of MRP1 have no statistical significance (P & gt;0.05) no matter after or before PHI was used on different concentration. Conlusion: The depletion effect of PHI on the intracellular GSH can not only partly enhance the reverse effect of ADM, but also enhance the sensitivity of K562/A02 cell line to ADM. Such depletion may diminish side effect and treatment dosage of ADM. It provides a new view to the therapy of leukaemia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5061.5061
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 5
    Online Resource
    Online Resource
    Effect of Cyclosporine A and Estrogen-Receptor Inhibitor on the Reversion of Multidrug Resistance of K562/A02 Line.
    American Society of Hematology ; 2006
    In:  Blood Vol. 108, No. 11 ( 2006-11-16), p. 4358-4358
    Details
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 4358-4358
    Abstract: Objective: This paper was to study the reverse effect of cyclosporine A and the estrogen-receptor inhibitor, raloxifene, on multidrug resistance cell line K562/A02 and to investigate the reversal mechanism of this combination, and to provide theoretic evidence for the clinical application of them as resistance modifying agents. Method: The IC50 (the concentration causing 50% inhibition of cell growth) of DNR were assayed by MTT method; mdr-1 mRNA was assayed by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).; intracellular DNR concentrations and the apoptosis and p-glycoprotein (p-gp) expression in K562 and K562/A02 were detected by fluorometry . Results: The IC50 of DNR for K562/A02 and K562 cells were 23.51mg/L and 0.29mg/L respectively. Pretreating K562/A02 cells with CsA(1mg/L) or raloxifene(2.5mg/L) for 48 hours partially restored the sensitivity of K562/A02 cells to DNR (IC50 were5.98mg/L and 8.15mg/L respectively) ,but had no effect on K562 cells;IC50 of combined cyclosporine A and raloxifene was 3.68mg/L The intracellular DNR concentrations( [DNR]i) in K562 cells were higher than that in K562/A02 cells,[DNR] i in K562/A02 cells was 12% of K562. Pretreating K562/A02 cells with cyclosporine A and raloxifene alone or combination for 48 hours induced the enhancement of [DNR]i in K562/A02 cells([DNR] i:CsA alone 33% of K562; raloxifene alone 12.78%of K562;CsA+raloxifene 45.29% of K562 Cyclosporine A and raloxifene alone or combination could decrease the expression of P-gp in K562/A02,the effect for 48 hours as follows: control(K562) 3.58,control(K562/A02) 104.96; CsA alone 78.29; raloxifene alone 85.02;CsA+raloxifene 59.89 K562/A02 showed apoptotic characteristics after treated with cyclosporine A for 48 hours and no apoptotic characteristics after treated with raloxifene for 48 hours Cyclosporine A and raloxifene alone could down regulate the expression of mdr-1 gene mRNA in K562/A02, cyclosporine A and raloxifene combination could markedly down regulate the expression of mdr-1 gene mRNA in K562/A02, the effect for 48 hours as follows(mdr1/β-action):control 1.313;CsA alone 1.232;raloxifene alone 1.052;CsA+raloxifene 0.449. Data was analyzed by SPSS 11.0 software and expressed as mean ± SD. Conclusions: Activation of P-gp may be involved in the mechanism of MDR of K562/A02 cell line; Multidrug resistance (MDR) can be partially reversed by CsA or raloxifene, of which the combination shows a great synergistic reversal effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V108.11.4358.4358
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2006
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 6
    Online Resource
    Online Resource
    Building and Clinical Use of Activated Plasma Clotting Time Test and the Value of APCT on Predicting the Bleeding Due to Leukemia Chemotherapy-Induced Thrombocytopenia.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 3915-3915
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 3915-3915
    Abstract: Objective This study was aimed to determine the optimal concertration of C-PG in activated plasma clotting time (APCT) test and build the APCT test.To investigate the value of activated plasma clotting time test (APCT) on predicting the bleeding due to Leukemia chemotherapy-induced thrombocytopenia. Method We collected healthy blood donors’venous blood, prepared watched platelet suspension and platelet rich plasma in a normal way to which we add different concertrations of C-PG, then test expression of AnnexinV in the surface of activated platelet by FCM. Prepared platelet rich plasma and platelet poor plasma in a normal way to which we add different concertrations of C-PG, then count the plasma clotting time.Forty-one patients with leukemia chemotherapy, twenty-one patients with petechiae or epistaxis or gum bleeding and twenty patients without bleeding symptoms, were involved in the test. Drawed their venous blood and collected in 3.2% buffered sodium citrate(9:1), the platelet counts and APCT, PT, APTT, TT, Fig were assesed. Result Bleeding group’s APCT was obviously prolonged contrast to the non-bleeding group’s. Platelet counts and APCT of the bleeding group and the non-bleeding group were (7.2±2.9) ×109/L, (105.9±8.1)s and (23.0±12.2) ×109/L,(71.4±9.0)s respectively. There was significant difference between the two groups (P & lt;0.01). Using APCT≥90s as the cut-off point to predict the bleeding caused by chemotherapy-induced thrombocytopenia, the sensibility was 100%, and the specificity was 95.7%. Using platelet counts ≤15*109/L, the sensibility and the specificity was 95.2% and 69.0%. PT, APTT, TT, Fig of the bleeding group and the non-bleeding group were 11.7±1.1)S,(31.5±1.3)S,(11.1±1.2)S,(2.37±0.41)g/L and (12.1±0.8)S,(30.8±2.1)S,(10.7±0.9)S,(2.64±0.27)g/L respectively. The results of the two groups were all not significantly different (P & gt;0.05). Conclusion APCT is a good indication of predicting the bleeding due to leukemia chemotherapy -induced thrombocytopenia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.3915.3915
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 7
    Online Resource
    Online Resource
    Reversal of Multidrug-Resistance in Human Leukemia Cell Line K562/A02 by Tyrosine Kinase Inhibitors.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 4828-4828
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4828-4828
    Abstract: Abstract 4828 Objective This study was aimed to investigate the reversible effect of tyrosine kinase inhibitors(TKI)on Multidrug resistance cell line K562/A02. Methods The expression levels of mdr-1 mRNA and bcr-abl mRNA were assayed by RT-PCR. The protein levels of P-glycoprotein (P-gp) and P210 were detected by Western blot. The DNR accumulation of K562/A02 cells were analyzed by flow cytometry (FCM). Results Analysis of the inhibition rate showed that 0.0625μmol/L Imatinib or 5nM Nilotinib alone had no effect on the inhibition of K562/A02 cells. The fluorescence intensity of intracellular DNR of Imatinib, Nilotinib in K562/A02 cells was 7.85%, 12.02% (respectively of that in K562 cells). Imatinib or Nilotonib alone could decrease the mdr-1 mRNA and bcr-abl mRNA expression levels (Imatinib 0.65±0.02, 0.87±0.02; Nilotinib 0.48±0.04, 0.73 ±0.02) respectively, all these of which were significantly lower than the K562/A02 cells group 0.96±0.01, 1.87±0.04. The P-gp and P210 protein expression levels were also down after treated with different drugs (Imatinib 0.74±0.02, 0.68±0.01; Nilotinib 0.61±0.05, 0.60±0.01; the K562/A02 cells group 0.93±0.01, 1.25±0.03). Conclusion It is concluded that multidrug resistance (MDR) can be partially reversed by Imatinib or Nilotinib. The effect of Nilotinib was greater than Imatinib. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.4828.4828
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 8
    Online Resource
    Online Resource
    In Vitro Study of the Effect of Cyclosporine A, Tetrandrine and Their Combination on the Reversion of Multidrug Resistance in Leukemia Cell Line.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4323-4323
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4323-4323
    Abstract: Objective: The aim of this study was to investigate the mechanism to reverse the drug resistance of leukemia cells in Cyclosporine A(CsA), tetrandrine (Tet) alone or their combination by using empirical methods, and to provide the basic evidence for further study, and lay the theoretical basis for the clinical applications. Method: By MTT assay, the IC50(the concentration causing 50% inhibitor of cell growth) of DNR was determined;By flow cytomet ry (FCM) assay, the intracellular DNR concentration and the expression of P-glyco-protein (P-gp) were examined, and the apoptotic changes were observed by Anexin-V. By fluorescent semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR), the mRNA expression of multidrug resistance (MDR) was measured. Results: The IC50 of DNR for K562 and K562/A02 cells were 0.26mg/l and 21.22mg/l respectively. Treating K562/A02 cells with CsA(1mg/L), TTD(0.1mg/L)and both for 48 hours partially restored the sensitivity of K562/A02 cells to DNR(IC50 were 7.83 mg/L,5.32 mg/L,2.33 mg/L respectively.) but had not effect on K562 cells; K562/A02 cells showed apoptotic characteristics after treated with CsA, and both for 48 hours(Apoptosis rate was 10.27%,17.64%,52.79% respectively); The fluorescence intensity of intracellelar DNR in K562 and K562/A02 cells treated with DNR(1mg/L)was 522,173 respectively. CsA and TTD (alone or combination) elevated the intracellular DNR concentration in K562/A02 cells(the fluorescence intensity of intracellelar DNR in K562/A02 cells was 188,339,515 respectively); The fluorescence intensity of P-gp in K562 and K562/A02 cells was 0.5,97.97. The P-gp expression was down after treated with CsA, TTD and both(73.7,65.05,58.1); mdr1 mRNA was also down regulated, and the effect of their combination was greater. Date was analyzed by SPSS 13.0 software and expressed as mean ± SD. Conclusions: High expression of P-gp may be involved in the mechanism of multidrug resistance (MDR) of K562/A02 cells line; MDR can be partially reversed by CsA or TTD, of which the combination shows a great synergistic reversal effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4323.4323
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 9
    Online Resource
    Online Resource
    Mechanism of Tetrandrine in Combination with Droloxifen To Reverse Multidrug Resistance in Leukemia.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4172-4172
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4172-4172
    Abstract: Objective: The study aims to investigate the effect of Tetrandrine (Tetrandrine, Tet) in combination with Droloxifen (Droloxifen, DRL) on the expression of NF-κB(nuclear factor kappaB) of K562 and K562/A02 cell lines and the reversal mechanism of this combination. Method: The activation of NF-κB in K562 and K562/A02 cell lines and the effect of Tet,DRL alone or in combination on NF-κB were determined with Immunocytochemistry and Western blotting respectively. Results: K562/A02 cells displayed higher level of NF-κB protein expression than their parental K562 cells; The application of Tet or DRL alone or in combination had no effect on NF-κB expression in K562 cells at 6h and 12h; Tet and DRL used alone or in combination could significantly down-regulate NF-κB protein expression in nucleaus of K562/A02 cells. The effect was more significant in combination of Tet and DRL than the application of single drug. This decrease became more significant at 12h than at 6h. Conclusions: Activation of NF-κB may be involved in the mechanism of MDR of K562/A02 cell line; Inhibition of NF-κB activation may be involved in the mechanism of multidrug resistance reversal to K562/A02 line of Tet and DRL.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4172.4172
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
    Online Resource
    Online Resource
    Identification of Transcription Factor AP-1 Bound to Untranslated 5′ Regulatory Region DNA of mdr1 Gene with Atomic Force Microscopy.
    American Society of Hematology ; 2006
    In:  Blood Vol. 108, No. 11 ( 2006-11-16), p. 4195-4195
    Details
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 4195-4195
    Abstract: Multidrug resistance(MDR) phenotype of cancer cells is a major obstacle for cancer chemotherapy, this phenotype is main due to the overexprssion of the mdr1 gene. Transcription factor AP-1, which is one of important regulate proteins in the promoter region of mdr1 gene. To date, no direct data of AP-1-DNA regulating complexes on mdr1 gene. A novel method for identifying DNA-binding proteins from image analysis using atomic force microscopy(AFM) was developed. This study is to image and map the structure of Untranslated 5′ regulatory region DNA of mdr1gene, identificate and analysis of transcription factor AP-1 bound to Untranslated 5′ regulatory region DNA of mdr1 gene complex with atomic force microscopy, to find out the molecule mechanism of multidrug resistance. Human leukemia adriamycin resistant strain K562/A02 was used as a target cells, transcription factor AP-1 was used as a target protein. Cultivate and PCR technique was used to amplify K562/A02 cells with the 769bp 5′regulatory region DNA of mdr1 gene, which fragment from −755 to +14. The amplified DNA products were purified by the PCR product purification kit, AP-1 of hela nuclear extract were purified by Sephadex spin-column filled with a bed of Sephadex G-100. The target DNA fragments were incubated with the target protein AP-1 at a 1:2 molar ratio in binding buffer and then immobilized the the AP-1-DNA complexes on a freshly cleaved mica surface which treated by MgCl2. AFM was used to idificate image of the structure of target DNA and the AP-1-DNA complexes. We show here the applicability of AFM in the quantitative analysis of the molecular mechanisms of DNA-protein interaction: The optimum DNA concentration to yield well-absorbed DNA molecular on the mica surface was found to be 10ng/ul. the contour of target DNA AFM image :the length of the DNA fragment measured by AFM image was 260.13± 2.29nm, the width was 11.88 ± 0.92nm, the mean height was 1.2nm(mean±SD, N = 50). Sephadex spin-column (Ultrafree- MC 0.22) can be used to purificate DNA and protein-DNA complex, the contour data of AP-1 protein AFM image:: the width of proteinlarge was 30±3.2nm, protein small was 19±2.8nm; the height of proteinlarge was 3.8±1.4nm, proteinsmall was 3.2±1.8nm (mean±SD, N = 30). we got the contour data of pro- tein-DNA complexes: the width of protein large was 28±2.7nm, the height was 3.4± 0.94nm (mean±SD, N = 8), the width of proteinsmall was 18±1.7nm, the height was 3.1±2.2nm (mean±SD, N = 22), and deduced the possible AP-1 site on mdr1DNA located between bases −126 and −115bp, this result is in close agreement with the expected −121 and −115 bp values. the overall connection efficiency of protein was about 10%. The AFM method to visualize individual biomolecules allows us to investigate the conformation of protein-DNA complexes.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V108.11.4195.4195
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2006
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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