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  • Zhao, Gang  (26)
  • Medicine  (26)
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  • Medicine  (26)
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  • 1
    Online Resource
    Online Resource
    Magnetic Nanoparticle of Fe3O4 Loaded with Daunorubicin Reverse Leukemia Multidrug Resistance in Vivo
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5062-5062
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5062-5062
    Abstract: Object: To the effect of Fe3O4-magnetic nanoparticle loaded with DNR on In order to study the multidrug-resistant reversal effect of Fe3O4-magnetic nanoparticle loaded with DNR in vivo. Methods: K562-n,a leukemia cell line with high tumorigenicity in nude mice and its multidrug-resistant counterpart K562-n/VCR cells were inoculated subcutaneously into each groins of nude mice (5×106 cells/each) to establish a human leukemia xenograft model. The mice were randomly divided into group A receiving normal saline, group B receiving anti-tumor drugs daunorubicin (DNR), group C receiving Fe3O4-magnetic nanoparticle, group D receiving Fe3O4-magnetic nanoparticle loaded with DNR, and group E receiving Fe3O4-magnetic nanoparticle containing DNR with a magnetic field built on the surface of tumor tissues. After 20 days treatments, mice were killed and tumor tissues were isolated for pathological observation. The volume and weight of tumors were measured, then tumor suppression rate was calculated. The side effects of DNR loaded Fe3O4-magnetic nanoparticle were also evaluated. Results: The results showed that DNR loaded Fe3O4-magnetic nanoparticle can significantly suppress the growth of K562-n/VCR tumor in vivo, DNR alone can greatly suppress the growth of K562-n, Fe3O4-magnetic nanoparticle loaded with DNR can not further inhibit the K562-n tumor. Conclusion: In conclusion, Fe3O4-magnetic nanoparticle loaded with DNR can reverse the leukemia multidrug resistance in vivo.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5062.5062
    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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  • 2
    Online Resource
    Online Resource
    Mechanisms of 2-Methoxyestradiol-Induced Apoptosis on Myelodysplastic Syndrome MUTZ-1 Cell Lines.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4590-4590
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4590-4590
    Abstract: Objective: To study the mechanism of proliferation inhibition and apoptosis of MDS-RAEB MUTZ-1 cells by 2-methoxyestradiol(2-ME). Methods: MUTZ-1 cells were treated with different concentrations of 2-ME;cellular proliferation was determined by MTT assay;apoptosis rate was determined with annexinV-FITC/PI double staining and cell cycle was analyzed by flow cytometry (FCM);the changes of morphologic features of MUTZ-1 cells were investigated by cytomorphology with Wright-Giemsa’s staining; lactate dehydrogenises (LD) was determined by Beckman Counter and agarose gel electrophoresis was used to verify whether 2-ME could induce apoptosis in MUTZ-1 cells. Moreover, the activity of telomerase in MUTZ-1 cells was examined by TRAP-ELISA. Results: The results showed that 1∼4μmol/L 2-ME inhibited the proliferation of MUTZ-1 cells in a dose-and time-dependent manner; the typical apoptotic morphological features appeared in MUTZ-1 cells after being treated with 4μmol/L 2-ME for 12hours; the marked DNA ladder pattern of internucleosomal fragmentation was observed after being treated with 4μmol/L 2-ME for 24hours and the up-regulated production of LD was assayed after treatment of 2-ME for 36hours. The number of MUTZ-1 cells of G0/G1 phase and S phase decreased, while the number of G2/M phase increased after MUTZ-1 cells were incubated with 1,2 and 4μmol/L2-ME for 12 hours, respectively(P 〈 0.05). The inhibition effect of telomerase activity was enhanced in a dose- and time- dependent manner. Moreover, telomerase activity was significant negatively correlated with increased apoptosis (r =−0.954, p=0.046) and the number of sustained G2/M phase(r=−0.979, p=0.021) at the corresponding time point, respectively. Conclusions :It is concluded that the mechanism of proliferation inhibition and apoptosis of MUTZ-1 cells induced by 2-ME is probably related with inhibition of telomerase activity and G2/M cell cycle arrest; 2-ME may be a potentially useful, adjunctive anticancer drug in treating myelodysplastic syndrome.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4590.4590
    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
    Daunorubicin Loaded Magnetic Nanoparticles of Fe3O4 Greatly Enhance the Responses to Chemotherapy and Induce Apoptosis of Multidrug-Resistant K562 Cells in a Human-Nude Mice Xenograft Leukemia Model
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5038-5038
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5038-5038
    Abstract: Object: To the effect of Fe3O4-magnetic nanoparticle loaded with DNR on multidrugresistant K562 cells in vivo. Methods: K562-n and its MDR counterpart K562-n/VCR cell were inoculated subcutaneously into both sides of the back of nude mice (5×106 cells/each) to establish a human leukemia xenograft model. The mice were randomly divided into group A receiving normal saline every other day for 20days, group B receiving DNR every other day for 20days, group C receiving Fe3O4-magnetic nanoparticle every other day for 20days, group D receiving Fe3O4-magnetic nanoparticle loaded with DNR every other day for 20days, and group E receiving Fe3O4-magnetic nanoparticle containing DNR every other day for 20days with a magnetic field built on the surface of the tumor tissue. The tumor volume was measured on the day 1, 5, 9, 13, 17 and 21d after the first treatment. Tumor tissues were isolated for examination of the expression of mdr-1, bcl-2, bax and caspase-3 by reverse transcription polymerase chain reaction and Western blotting. Results: For K562-n/VCR tumor, the tumor volume was markedly lower in groups D and E than in groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). The transcription of mdr-1 and Bcl-2 gene was significantly lower in groups D and E than in groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). So did the protein expression of Bcl-2. However, there were no differences among these groups about the protein expression of P-gp. The protein and mRNA expressions of Bax and Caspase-3 in groups D and E were increased significantly compared with groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). The tumor volume of K562-n was markedly lower in groups C, D and E than in groups A and B (group C, D or E vs group A or B, P & lt; 0.05). Conclusion: In conclusion, DNR loaded Fe3O4-magnetic nanoparticles can suppress the growth and induce apoptosis further on the MDR K562-n/VCR tumor in vivo compared to DNR alone but not on the K562-n tumor. The external magnetic field failed to improve the antitumor effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5038.5038
    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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  • 4
    Online Resource
    Online Resource
    Effects of Sodium Valproate on Proliferation and Apoptosis of Human Myelodysplastic Syndromes Cell Line MUTZ-1.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4090-4090
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4090-4090
    Abstract: OBJECTIVE: Myelodysplastic syndromes (MDS) are a heterogeneous group with the expansion of a malignant clone. No satisfactory treatment for MDS is available. Sodium valproate (VPA), can induce G0–G1 phase arrest and cell apoptosis, inhibit proliferation of tumor cells in vitro significantly. The effects and possible mechanism of VPA on MUTZ-1 cell line of MDS were studied in this experiment. METHODS: Cell proliferation was determined by MTT assay. Apoptotic morphological features were observed under microscope and transmission electronmicroscope. Cell apoptosis and cell cycle were analyzed by flow cytometry (FCM). The expression of p21WAF1(cyclin-dependent kinase inbihitor) was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. RESULTS: VPA could inhibit the proliferation of MUTZ-1 cells in dose-and time-dependent manners. The typical apoptotic morphological features appeared in cells treated with 4 mmol/L VPA for 72 hours. Condensation of cells and nuclear chromatin, disintegration of nuclear chromatin, and apoptotic body could be observed under microscope. Aggregation and margination of apoptotic nuclear chromatin, cytoplasm condensation, and irregular chromatin masses could be observed under transmission electronmicroscope. The percentage of apoptotic cells which were treated with 1,2 and 4 mmol/L VPA for 72 hours increased from 1.39% to 2.18%, 16.03%, 22.02%, and cell cycle arrest at G0–G1 phase could be caused by VPA as shown by FCM. The expression level of p21WAF1 mRNA and p21WAF1 protein were up-regulated in a dose dependent manner in MUTZ-1 treated with VPA for 72 hours (P 〈 0.05). CONCLUSION: VPA induced a G0–G1 cell cycle arrest and have an effect on proliferation and apoptosis of MUTZ-1 cells in vitro. The mechanism may be associated with the up-regulation of p21WAF1.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4090.4090
    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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  • 5
    Online Resource
    Online Resource
    Fecal Signatures of Streptococcus anginosus and Streptococcus constellatus for Noninvasive Screening and Early Warning of Gastric Cancer
    Elsevier BV ; 2022
    In:  Gastroenterology Vol. 162, No. 7 ( 2022-06), p. 1933-1947.e18
    Details
    In: Gastroenterology, Elsevier BV, Vol. 162, No. 7 ( 2022-06), p. 1933-1947.e18
    Type of Medium: Online Resource
    ISSN: 0016-5085
    URL: Article
    DOI: 10.1053/j.gastro.2022.02.015
    RVK:
    XA 44500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
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  • 6
    Online Resource
    Online Resource
    Effect of PDMP, a Glucosylceramide Synthase Inhibitor, On Resistance to Daunorubicin in Human Leukemia Cell Line K562/A02.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 4821-4821
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4821-4821
    Abstract: Abstract 4821 Objective Previous studies showed inhibition of glucosylceramide synthase (GCS) increased sensitivity to doxorubicin toxicity in multidrug-resistant cancer cells. This study was purposed to investigate the reversal effect of D, L-threo-1-phenyl-2- -decanoylamino-3-morpholino-1-propanol (PDMP), a glucosylceramide synthase inhibitor, on daunorubicin (DNR) resistance in K562/A02 cells. Material and methods The cytotoxicity and reversal effect were analyzed by MTT method. Flow cytometry was used to test DNR accumulation and apoptosis percentage. The expressions of GCS and mdr1 genes of K562 and K562/A02 cells were measured by RT-PCR and Western blot. Results The inhibition rates of PDMP (≤20μmol/l) on the proliferation of K562 and K562/A02 cells were below 10%. The IC50 of DNR for K562 and K562/A02 cells were 0.23±0.02μg/ml and 7.15±0.24μg/ml, respectively. PDMP increased sensitivity of K562/A02 cells to DNR toxicity in a dose-dependent manner (the IC50 was decreased to 2.76±0.25μg/ml by 20μM PDMP and to 4.23±0.08μg/ml by 10μM PDMP), but it had no effect on K562 cells. Both 10μM and 20μM PDMP increased DNR induced apoptosis compared with DNR alone (the apoptosis percentage were 8.93%±0.83%, 18.33% ± 0.86%and 5.43% ± 0.70% respectively). The mean fluorescence intensity of DNR in K562/A02 cells increased from 1550 treated by DNR alone to 1631 incubating with 10μM PDMP and higher to 1998 by 20μM PDMP. The expression of GCS gene was down-regulated by 20μM PDMP and blocking GCS also showed a dramatic decrease in mdr1 expression. Conclusion PDMP can increase the sensitivity to DNR toxicity in K562/A02 cells by enhancing cell apoptosis rate, intracellular DNR concentration, and down-regulating expressions of both GCS and mdr1 genes. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.4821.4821
    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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  • 7
    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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  • 8
    Online Resource
    Online Resource
    Effect of YC-1, a HIF Inhibitor,On Apoptosis of Leukemia Cell.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 4432-4432
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4432-4432
    Abstract: Abstract 4432 Object This study was purposed to investigate the expression of HIF-1α and VEGF in leukemia cell lines and the effect of YC-1 on the regulation of HIF-1α and VEGF and the induction of apoptosis in U937 cell, exploring the mechanism of apoptosis after treatment of YC-1. Methods RT-PCR was used to determine the levels of HIF-1α mRNA and VEGF mRNA in K562,U937 and Jurkat cells. After treatment of U937 cell with 4μmol/L YC-1 for 0 hour, 8 hours,16 hours and 24 hours respectively, the changes of morphologic features were observed by DAPI staining under fluorescent microscope and the apoptotic rates were assayed by flow cytometry with Annexin V-FITC/PI staining; the levels of HIF-1α mRNA and VEGF mRNA were measured with RT-PCR ; the protein expression of HIF-1α, VEGF, Bax,Bcl-2 and Caspase-3 were measured by Western blot. Results HIF-1α mRNA and VEGF mRNA were expressed in all three leukemia cell lines. After treatment of U937 cell with 4μmol/L YC-1 for 0 hour,8 hours,16hours and 24hours respectively, the typical apoptotic morphologic features of U937 cells were observed under fluorescent microscope and the apoptotic rates were significantly increased in a time-dependent manner, they were (4.87±0.70)%, (27.27±2.00)%, (51.53±2.81) and (60.5±3.20)% respectively, the level of VEGF mRNA reduced, while the level of HIF-1α mRNA had no obviously changes. Furthermore, the expression of HIF-1α, VEGF and Bcl-2 decreased, while the expression of Bax and Caspase-3 increased in a time-dependent manner. Conclusion HIF-1α mRNA and VEGF mRNA are expressed in leukemia, YC-1 has significant effect of down-regulation the protein expression of HIF-1α and VEGF and induction of apoptosis in U937, its mechanisms may involve in up-regulating Bax/Bcl-2 ratio and expression of Caspase-3. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.4432.4432
    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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  • 9
    Online Resource
    Online Resource
    Variation of Sorcin’s Expression in the Reversion of Multidrug Resistance of K562/A02 Leukemic Line with Tetrandrine.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4176-4176
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4176-4176
    Abstract: Objective This paper aims to investigate the reversal multiple of daunomycin(DNR) with different concentration of tetrandrine(tet) at different time, to study the variation of Soluble resistance related calcium binding protein (sorcin)’s expression in the reversion of multidrug resistance of K562/A02 leukemic line with different concentration of tet at different time, and to provide new theoretic evidence for the clinical application of tet as resistence modifying agents. Method The reversal multiple of DNR with different concentration of tet at different time was assayed by MTT (concentration of tet is 0.5mg/l or1mg/l or 2mg/l, incubation time is 48h or 72h). The variation of the gene’s expression of sorcin with different concentration of tet at different time wasassayed by RT-PCR(grouping like MTT). Result MTT analysis demonstrated that the reversal concentration was 1.81(0.5mg/l,48h),3.62(1.0mg/l,48h),6.14(2.0mg/l,48h),2.8(0.5mg/l,72h),(1.0mg/l,48h),7.12(2.0mg/l,72h) respectively. RT-PCR analysis demonstrated that sorcin gene was lowly displayed in K562 cells and highly displayed in K562/A02 cells. The variation was first accentuation and then attenuation with the concentration accrescence of tet, this tendency had no obviously difference between 48h and 72h. Conclusion 1 The result of the experiment shows that tet may reverse multidrug resistance of K562/A02 cells by the down regulation of the expression of sorcin gene and proteinum; 2. It may have the concentration dependence and the time dependence in the reversion of multidrug resistance of K562/A02 cells with tet.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4176.4176
    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
    Molecular Biological Mechanisms of Cyclosporine a, Tetrandrine and Their Combination on the Reversion of Multidrug Resistance in Leukemia Cell Line
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5065-5065
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5065-5065
    Abstract: Objective Previous researches confirmed that multidrugresistance(MDR) plays an important role in the failure of chemotherapy on malignant tumors. This study was to investigate the molecular biological mechanisms of cyclosporine A(CsA), tetrandrine(Tet) and their combination on multidrug resistance cell line K562/A02. Methods K562/A02 cells were treated with cyclosporine A and (or) tetrandrine. The intracellular DNR concentration and the expression of P-glyco-protein (P-gp) were observed by flow cytometry (FCM) assay. The mRNA expression of mdr-1 was measured by fluorescent semi-quantitative reverse transcriptase polymerase chain reaction(RT-PCR). Resulds CsA and Tet (alone or combination) elevated the intracellular DNR concentration in K562/A02 cells(the fluorescence intensity of intracellelar DNR in K562/A02 cells was 60%,65% and 98% respectively of that in K562 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 CsA,Tet and both(75.32%,76.86% and 48.61%); mdr1 mRNA was also down regulated, and the effect of their combination was greater. Conclusion Multidrug resistance (MDR) can be partially reversed by CsA or Tet, the combination of both drugs shows a great synergistic reversal effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5065.5065
    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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