Wei-Ke Cao

Nanjing Medical University, Nan-ching, Jiangsu Sheng, China

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Publications (6)0 Total impact

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    ABSTRACT: This study was aimed to explore the change of K562 cell apoptosis at different time point after homoharringtonine (HHT) treatment and its mechanism. After treatment of K562 cells with 10 ng/ml HHT, the cell viability was tested with MTT assay; the expression of caspase-3 was detected with Western blot; the BCL-2 expression was analyzed with flow cytometry; the autophagosome was observed by electron microscopy. The results showed that the viability of K562 cells reduced gradually from day 1 to day 5 and ascended from day 6 to day 8 after HHT treatment. At the same time, the cleaved caspase-3 expression level of K562 cells increased gradually from day 1 to day 7, but reduced at the day 8 (P < 0.05). From day 1 to day 8 after HHT treatment, the BCL-2 expression level declined firstly and then went up (P < 0.05). Autophagosome was also seen remarkably at day 8 after HHT treatment. It is concluded that the apoptosis level of K562 cells after being treated with HHT enhances firstly and then declines , which may be associated with higher autophage level in the late stage of HHT treatment.
    05/2014; 22(3):712-6.
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    ABSTRACT: This study was aimed to investigate the effect of homoharringtonine (HHT) on K562 cell proliferation, apoptosis and expression of BCL-2 and NF-κB proteins. The cells proliferation was assayed with MTT method, the cell apoptosis, cell cycle and BCL-2 expression were analyzed with flow cytometry, NF-κB protein expression was detected with Western blot. The results showed that HHT concentration-denpendently inhibited proliferation of K562 cells, the IC50 at 48 h was 43.89 ng/ml. Treated with HHT 10 ng/ml for 48 h, K562 cell apoptosis significantly increased, cell cycle was blocked at G0/G1, the expression level of BCL-2 and NF-κB proteins was lower than that in control group (P < 0.05). It is concluded that HHT may inhibit the proliferation of K562 cells, and down-regulating expression levels of BCL-2 and NF-κB may be one of its anti-CML mechanisms.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 01/2013; 21(1):78-81.
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    ABSTRACT: The study was aimed to investigate the synergistical effect of interferon-α (IFN-α) and homoharringtonine (HHT) on the proliferation, apoptosis, cell cycle of K562 cells and the expression of β-catenin. The proliferation, apoptosis, cell cycle and β-catenin mRNA expression of K562 cells treated with IFN-α and/or HHT were assayed with MTT, flow cytometry or RT-PCR respectively. The results showed that HHT alone, but not IFN-α alone, displayed a proliferation inhibition, apoptosis induction, G(0)/G(1) phase block and down-regulation of β-catenin expression in K562 cells with concentration- and time-dependent manners. The expression level of β-catenin mRNA after being treated with HHT was 0.5576 ± 0.0373, which were lower than that in control group (0.9369 ± 0.0142). The down-regulation of β-catenin expression in group of IFN-α combined with HHT was higher significantly than that in HHT group (0.3737 ± 0.0529 vs 0.5576 ± 0.0373, P < 0.05). Otherwise, HHT combined with IFN-α did not demonstrate obvious toxicologic effect on bone marrow mononuclear cells. It is concluded that IFN-α combined with HHT can enhance the cytotoxic effect of HHT on K562 cells, which may be associated with down-regulation of β-catenin expression.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 01/2012; 20(1):43-7.
  • Hua Guo, Wei-Ke Cao, Ding-Sheng Liu
    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 06/2011; 32(6):408-9.
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    ABSTRACT: The aim of this study was to investigate the effects of Celecoxib on the proliferation, apoptosis, cell cycle and CD117 expression of K562 cells, and to explore its synergistic effect with IFN-alpha. K562 cells were treated with IFN-alpha, Celecoxib and combination of Celecoxib with IFN-alpha at different concentrations. The inhibitory effect of Celecoxib and IFN-alpha on cell proliferation was detected with MTT assay, the cell apoptosis, cell cycle and CD117 expression were determined by morphology observation and flow cytometry. The results showed that the Celecoxib inhibited proliferation of K562 cells in concentration-dependent manner (r=-0.91). After culture of K562 cells for 72 hours, the rates of K562 cell proliferation in control group, IFN-alpha group, Celecoxib group and IFN-alpha-combined Celecoxib group were (96.1+/-0.5)%, (90.2+/-0.4)%, (57.2+/-0.9)% and (21.9+/-0.3)% respectively. The cell apoptosis rates in 4 groups were (5.5+/-0.8)%, (6.3+/-0.6)%, (26.4+/-3.9)% and (57.3+/-4.5)% respectively. The CD117 expression rates in 4 groups were 54.7%, 10.5%, 36.3% and 7.3% respectively. Combination of Celecoxib with IFN-alpha might block K562 cells in G0/G1 phase. In conclusion, Celecoxib and IFN-alpha both may inhibit K562 cell proliferation, induce apoptosis, reduce CD117 expression and produce G0/G1 phase block to various degree and the two drugs have a synergistic effect.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 04/2010; 18(2):330-4.
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    ABSTRACT: To study the effect of allicin on invasion and metastasis of human colon cancer cell line LoVo in vitro and furthermore elucidate its anticancer mechanisms. MTT assay was used to test dynamically the effect of cell growth inhibition. The inhibitory effects of allicin on movement, adhesiveness and invasiveness of LoVo cells were evaluated by the migratory test, adhesion test and Transwell chamber experiment. Quantitative real-time reverse transcription PCR (real-time RT-PCR) was performed to quantify the mRNA expression of MMP-2, TIMP-2, CD147, VEGF, nm23-H1, HPA and uPAR. Allicin had inhibitive effects on growth of LoVo cells in a dose and time-dependent manner. Allicin at non-cytotoxic concentration (3 and 6 microg/ml) could obviously suppress the movement, adhesion and invasive capability of LoVo cells. In the allicin-treated group (3 and 6 microg/ml), after 24 hours, the inhibition rates of migratory time were 24% and 50% (t = 4.543, 12.348, P = 0.010, 0.001), the inhibition rates of adhesion were 19% and 28% (t = 6.145, 6.355, P = 0.004, 0.003), the inhibition rates of migration were 28% and 46% (t = 8.065, 28.435, both P < 0.01), and the inhibition rates of invasion were 44% and 65% respectively (t = 21.274, 26.288, both P < 0.01). Allicin at non-cytotoxic concentration could down-regulate the mRNA levels of VEGF, uPAR and HPA in a dose-dependent manner in LoVo cells (t = 7.129, 6.764, 8.497, P = 0.002, 0.002, 0.001) while the mRNA levels of TIMP-2, CD147 and nm23-H1 remained basically unchanged with the same treatment (t = 0.341, 1.889, 0.914, P = 0.059, 0.132, 0.412). The expression of MMP-2 had not been detected in LoVo cells. Allicin in vitro inhibits invasion and metastasis of human colon carcinoma cell LoVo at non-cytotoxic concentration through down-regulating the expression of VEGF, uPAR and HPA mRNA.
    Zhonghua yi xue za zhi 06/2009; 89(20):1382-6.