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1.
Journal of Leukemia & Lymphoma ; (12): 535-538, 2015.
Article in Chinese | WPRIM | ID: wpr-479907

ABSTRACT

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.

2.
Journal of Leukemia & Lymphoma ; (12): 261-265, 2011.
Article in Chinese | WPRIM | ID: wpr-471743

ABSTRACT

Objective To explore the effects and the possible molecular mechanism of flavonoids of puerarin (PR) on chronic myelogenous leukemia (CML) cell line K562 and acute promyelocytic leukemia (APL) cell line NB4 in vitro. Methods MTT assays were used to detect the inhibitory effects of cell proliferation. The apoptosis of K562 and NB4 cells was detected by flow cytometry marked with Annexin V/PI. The expression of bcr-abl, p53, bcl-2, Fas/FasL in K562 cells and JNK, PARP, bcl-2 and Caspase 3 in NB4 cells at protein level was detected by Western blot. Results PR could inhibit the proliferation of K562 and NB4 cells in a time-dose dependent manner. The expression of protein levels of bcr-abl fusion gene declined, while the p53 protein otherwise increased, and both were in a dose-dependent manner (F = 18.74, P <0.05). The application of PR had no effect on bcl-2 and Fas/FasL protein expression in K562 cells. The JNK, PARP and Caspase3 proteins were upregulated in NB4 cells, while bcl-2 was downregulated with the increasing concentrations of PR (F=42.32, P <0.05). Conclusion PR could inhibit leukemic cell proliferation, induce cell cycle block, and increase cell apoptosis through different molecular mechanisms. It suggestes that PR might potentially be a kind of broad spectrum anti-leukemia agent.

3.
Chinese Journal of Cellular and Molecular Immunology ; (12): 900-902,906, 2009.
Article in Chinese | WPRIM | ID: wpr-625055

ABSTRACT

AIM: To explore the different effect and mechanism of arsenic sulfide on telemorase activity and hTERT-mRNA expression in CML cell lines-KS62 and APL cell lines-NB4. METHODS: Telomerase activity was determined by polymerase chain reaction enzyme-linked immunoassay (PCR-ELISA). The expression of hTERT-mRNA was analyzed by semi-quantitative RT-PCR. Flow cytometry was used to analyze the cell cycle and apoptosis. RESULTS: 0.15-0.6 mg/L arsenic sulfide (72 h)can induce apoptosis and inhibit telomerase activity and hTERT-mRNA expression in NB4 cell. The concentration of arsenic sulfide with the same effect on K562 cell was 0.3-3 mg/U 0.3 mg/L arsenic sulfide (72 h) can cause the proportion of the NB4 cell in G2/M phase increased, but for K562 cell, The concentration of arsenic sulfide was 1.5 mg/L. CONCLUSION: Telomerase system may be one.of the pathway for arsenic sulfide inducing apoptosis of NB4 and K562 cell; G2/M phrase arrest may have correlation with decrease of telomerase activity; The sensitivity of NB4 and K562 call for arsenic sulfide is different, the mechanism of it need to study more.

4.
Journal of Leukemia & Lymphoma ; (12): 412-414, 2008.
Article in Chinese | WPRIM | ID: wpr-473225

ABSTRACT

Objective To explore molecular mechanisms of apoptosis induced by STI571 in human acute promyelocytie 1eukemia cell lines NB4.nethods The expression of Annexin-V,Fas,Caspase-3 and bcl-2 in NB4 cells were detected by FCM after the treatment of STI571 at(0.5,1.0,5.0 μmol/L)ranging for 24 h,48 h and 72 h.Results With the increasing dose of STI571,the expression of bcl-2,Caspase-3,Annexin-V,Fas in NB4 changed from(10.22±0.62)declining to (5.82±0.52),from(42.21±1.02)ascending to(52.35±0.83),from(25.A2±1.21)ascending to(37.84±0.63),from(18.21±0.81)to(21.41±1.02)respectively.With the dealing time increasing(24,48,72 h),the expression of bcl-2,Caspase-3,Annexin-V,Fas in NB4,changed from (5.81±0.52)declining to(2.51±0.43),from(52.31±0.83)ascending to(69.51±1.12),from(37.81±0.93)ascending to(78.62±0.83),from(23.41±0.73)to(26.53±1.02)respectively.Conclusion STI571 can enhance the apoptosis program to Ni4 in a time-dependence and dose-dependence manner,but no change to Fas was observed.

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