Publications by authors named "Wei-Ke Cao"

7 Publications

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[Time rhythm of homoharringtonine inducing K562 cell apoptosis and its mechanism].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2014 Jun;22(3):712-6

Department of Hematology, Huai'an First People's Hospital, Nanjing Medical University, Huaian 223300, Jiangsu Province, China. E-mail:

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 autophagy level in the late stage of HHT treatment.
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http://dx.doi.org/10.7534/j.issn.1009-2137.2014.03.026DOI Listing
June 2014

[Effect of homoharringtonine on expression of NF-κB and BCL-2 proteins in K562 cells].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2013 Feb;21(1):78-81

Department of Hematology, Nanjing Medical University, Huaian, Jiangsu Province, China.

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-dependently 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.
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http://dx.doi.org/10.7534/j.issn.1009-2137.2013.01.017DOI Listing
February 2013

[Effects of interferon-α combined with homoharringtonine on K562 cell proliferation and β-catenin expression].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2012 Feb;20(1):43-7

Department of Hematology, Nanjing Medical University, Huaian, Jiangsu Province, China.

The study was aimed to investigate the synergistically 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.
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February 2012

Genome-wide association study of esophageal squamous cell carcinoma in Chinese subjects identifies susceptibility loci at PLCE1 and C20orf54.

Nat Genet 2010 Sep 22;42(9):759-63. Epub 2010 Aug 22.

Cancer Research Center, Xinxiang Medical University, Xinxiang, Henan, China.

We performed a genome-wide association study of esophageal squamous cell carcinoma (ESCC) by genotyping 1,077 individuals with ESCC and 1,733 control subjects of Chinese Han descent. We selected 18 promising SNPs for replication in an additional 7,673 cases of ESCC and 11,013 control subjects of Chinese Han descent and 303 cases of ESCC and 537 control subjects of Chinese Uygur-Kazakh descent. We identified two previously unknown susceptibility loci for ESCC: PLCE1 at 10q23 (P(Han combined for ESCC) = 7.46 x 10(-56), odds ratio (OR) = 1.43; P(Uygur-Kazakh for ESCC) = 5.70 x 10(-4), OR = 1.53) and C20orf54 at 20p13 (P(Han combined for ESCC) = 1.21 x 10(-11), OR = 0.86; P(Uygur-Kazakh for ESCC) = 7.88 x 10(-3), OR = 0.66). We also confirmed association in 2,766 cases of gastric cardia adenocarcinoma cases and the same 11,013 control subjects (PLCE1, P(Han for GCA) = 1.74 x 10(-39), OR = 1.55 and C20orf54, P(Han for GCA) = 3.02 x 10(-3), OR = 0.91). PLCE1 and C20orf54 have important biological implications for both ESCC and GCA. PLCE1 might regulate cell growth, differentiation, apoptosis and angiogenesis. C20orf54 is responsible for transporting riboflavin, and deficiency of riboflavin has been documented as a risk factor for ESCC and GCA.
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http://dx.doi.org/10.1038/ng.648DOI Listing
September 2010

[Influence of celecoxib combined with IFN-alpha on proliferation, apoptosis, cell cycle and CD117 expression of K562 cells].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2010 Apr;18(2):330-4

Department of Hematology, The First Huaian People Hospital, Nanjing Medical University, Huaian 223300, Jiangsu Province, China.

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.
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April 2010

[Effects of allicin on invasion and metastasis of colon cancer LoVo cell line in vitro].

Zhonghua Yi Xue Za Zhi 2009 May;89(20):1382-6

Department of Oncology, Affiliated Huai'an No.1 Hospital of Nanjing Medical University, Huai'an 223300, China.

Objective: 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.

Methods: 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.

Results: 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.

Conclusion: 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.
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May 2009