Mei-Xiang Sang

Hebei Medical University, Chentow, Hebei, China

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Publications (7)6.39 Total impact

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    ABSTRACT: Decitabine, a demethylating drug, is the first-line treatment for myelodysplastic syndromes and gains better overall survival, which is based on epigenetic mechanism. Activated by promoter demethylation, melanoma-associated antigens-A (MAGE-A), cancer-testis antigens are attractive targets for immunotherapy. Our purpose was to investigate whether decitabine could show anti-tumor effects for esophageal cancer and explore its mechanism. In addition, we aimed to examine its modulation for most MAGE-A members. The results showed the baseline expression were MAGE-A2, -3,-9, and -10 in Eca109 cells and decitabine (0.5 μM) could induce MAGE-A8 and -4 whereas reduce MAGE-A9 and -10. Moreover, decitabine (0.5 μM) inhibited cell proliferation, migration and invasive ability by 15%, 34% and 47.2%, respectively and decreased expressions of NF-κB2 and MMP2. Our results demonstrated that low-dose decitabine induced the expression of MAGE-A8 and -4, and inhibited cell invasion through decreasing expression of MMP2 and NF-κB2, which provides possibilities for combing decitabine with immunotherapy targeting MAGE-A to treat advanced esophageal squamous cell carcinoma.
    Biomedicine & Pharmacotherapy. 01/2014;
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    ABSTRACT: The MAGE gene encodes cancer/testis antigens that are selectively expressed in various types of human neoplasms but not in normal tissues other than testis and placenta. However, the expression pattern of MAGE-A9 and MAGE-A11 in breast cancer patients is still unclear. The purpose of our study is to investigate the expression pattern and mechanism of MAGE-A9 and MAGE-A11 in breast cancer patients. The expression of MAGE-A9 and MAGE-A11 was investigated in 60 breast benign diseases specimens, 60 tumor-free breast specimens and 60 breast cancer specimens by RT-PCR, and their correlation with clinicopathological parameters was elucidated. We examined the influence of the DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) together with the histone deacetylase inhibitor trichostatin A (TSA) on the expression of MAGE-A9 and MAGE-A11 genes in two breast cancer cell lines. The expression rates of MAGE-A9 and MAGE-A11 in breast cancer specimens were 45 and 66.7%, respectively. MAGE-A9 and MAGE-A11 expression was positively associated with estrogen-receptor (ER) and HER-2 expression (p <0.05). 5-Aza-CdR treatment alone could induce the expression of MAGE-A9 and MAGE-A11 in cell lines that did not express this antigen. TSA treatment alone had no influence on MAGE-A9 and MAGE-A11 gene expression. However, TSA was able synergistically to enhance 5-aza-CdR-mediated MAGE-A transcription (p <0.05). Our data show that MAGE-A9 and MAGE-A11 are tumor-specific antigens and not only DNA hypermethylation but also histone deacetylation is responsible for the mechanism underlying MAGE-A9 and MAGE-A11 gene silencing.
    Archives of medical research 12/2013; · 1.88 Impact Factor
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    ABSTRACT: Cochinchina momordica seeds (CMS) have been widely used due to antitumor activity by Mongolian tribes of China. However, the details of the underlying mechanisms remain unknown. In the present study, we found that an EtOAc (ethyl ester) extract of CMS (CMSEE) induced differentiation and caused growth inhibition of melanoma B16 F1 cells. CMSEE at the concentration of 5-200 μg/ml exhibited strongest anti-proliferative effects on B16 F1 cells among other CMS fractions (water or petroleum ether). Moreover, CMSEE induced melanoma B16 F1 cell differentiation, characterized by dendrite-like outgrowth, increasing melanogenesis production, as well as enhancing tyrosinase activity. Western blot analysis showed that sustained phosphorylation of p38 MAP accompanied by decrease in ERK1/2 and JNK dephosphorylation were involved in CMSEE-induced B16 F1 cell differentiation. Notably, 6 compounds that were isolated and identified may be responsible for inducing differentiation of CMSEE. These results indicated that CMSEE contributes to the differentiation of B16 F1 cells through modulating MAPKs activity, which may throw some light on the development of potentially therapeutic strategies for melanoma treatment.
    Asian Pacific journal of cancer prevention: APJCP 01/2012; 13(8):3795-802. · 1.50 Impact Factor
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    ABSTRACT: To explore the effect of microRNA (miRNA)-mediated p65 gene knockdown on the proliferation and apoptosis of human breast cancer MDA-MB-231 cells. p65-targeted miRNA plasmid was constructed and transfected into MDA-MB-231 cells via lipofectamine(TM)2000. The expression of p65 gene in the transfected cells at the mRNA and protein levels were detected by RT-PCR and Western blotting, respectively. The cell proliferation and apoptosis were measured by MTT assay and flow cytometry (FCM), respectively. The expressions of apoptosis-related proteins were detected by Western blotting in the transfected cells. Compared with the negative control group, the expressions of p65 mRNA and protein in p65miRNA-trasnfected cells were significantly down-regulated (P<0.05). MTT assay showed significantly lowered viability of MDA-MB-231 cells after the transfection (P<0.05). FCM showed an increased cell apoptosis rate in p65miRNA group compared with that in the negative control group (P<0.05). Caspase-3 and PARP were both cleaved into their active forms and the expression of these active forms was increased in p65miRNA group. The miRNA targeting p65 gene can inhibit the proliferation and induce apoptosis of breast cancer cells, and p65 gene might become a new target in gene therapy for human breast cancer.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 10/2011; 31(10):1742-7.
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    ABSTRACT: Currently, no satisfactory biomarkers are available to screen for esophageal squamous cell carcinoma (ESCC). The goal of this study was to find biomarkers and establish a serum protein fingerprint model for early diagnosis of ESCC using the ClinProt protocol of matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Serum samples were collected from 62 patients with ESCC, nine patients with esophageal adenocarcinoma (EA) and 38 healthy individuals. Proteomic spectra of mass to charge ratio (m/z) were generated following the application of plasma to weak cationic-exchanger magnetic beads (WCX-MB). The spectral data were analyzed using a support vector machine, and potential biomarkers were chosen for system training and used to construct diagnostic models. Three differential patterns were established using MALDI-TOF MS. Pattern 1, consisting of 11 protein peaks, separated ESCC patients from the healthy individuals with a sensitivity of 90.0% and a specificity of 88.4%. Pattern 2, consisting of eight protein peaks, separated ESCC in stage I and stage II from stage III and stage IV with a sensitivity of 92.9% and a specificity of 82.3%. Pattern 3, consisting of seven protein peaks, separated ESCC from EA with a sensitivity of 91.3% and a specificity of 80.0%. These results suggested that MALDI-TOF MS combined with MB separation yields significantly higher sensitivity and specificity for the detection of serum protein in patients with ESCC.
    Clinical Chemistry and Laboratory Medicine 03/2010; 48(6):855-61. · 3.01 Impact Factor
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    ABSTRACT: Celecoxib can inhibit cell proliferation, regulate cell cycle and induce apoptosis, but the underlying mechanisms are still unclear. This study was to investigate the association between the NF-kappaB (kappaB) pathway and the apoptosis of breast cancer cell line MDA-MB-231 induced by celecoxib. The expression of cyclo-oxygenase-2 (COX-2) mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Cell proliferation and cell cycle were detected by MTT and flow cytometry (FCM), respectively. The protein expressions of caspase-3 and p65 in MDA-MB-231 cells were detected by western blot. After incubation with different concentrations of celecoxib for 48 h, COX-2 mRNA expression in MDA-MB-231 cells was decreased in a dose-dependent manner compared with untreated cells (P<0.05). Proliferation of MDA-MB-231 cells was reduced drastically in a dose-and time-dependent manner after celecoxib treatment (P<0.05). Combination of prostaglandin E2 (PGE2) and celecoxib exerted similar inhibition effect to celecoxib alone on cell growth (P>0.05). High-dose celecoxib induced an increase in the percentage of G0/G1 phase cells accompanied by the change in DNA ploidy. The cellular caspase-3 level was enhanced whereas the p65 level was decreased in celecoxib-treated MDA-MB-231 cells after 24 h in comparison to those in the control cells. Celecoxib could inhibit MDA-MB-231 cell proliferation and promote cell apoptosis by down-regulating the NF-kappaB signaling pathway.
    Ai zheng = Aizheng = Chinese journal of cancer 06/2009; 28(6):569-74.
  • Mei-Xiang Sang, Cui-Zhi Geng, Bao-En Shan
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    ABSTRACT: p53 gene is the main regulator of 14-3-3sigma. Activated p53 could induce the expression of 14-3-3sigma, while 14-3-3sigma stabilizes the expression of p53 and enhances its transcriptional activity. p63 and p73, the members of p53 family, also have some functions similar to p53. This study was to investigate the effect of 14-3-3sigma on the transcriptional activity of p73. Luciferase reporter assay, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot were used to evaluate the effect of 14-3-3sigma on the transcriptional activity of p73 in p53-deficient human lung carcinoma cell line H1299. Colony formation test was used to evaluate the effect of 14-3-3sigma on the transcriptional activity of p73 in p53-mutant human breast cancer cell line MDA-MB-436. The luciferase activities induced by bax and p21WAF1 promotors were significantly higher in p73-transfected H1299 cells than in control H1299 cells (P<0.01), and were further increased by the transfection of p73 (25 ng) and 14-3-3sigma (100, 200, and 400 ng) in a dose-dependent manner (P<0.01). The expression of bax and p21WAF1 were higher in p73-transfected H1299 cells than in control H1299 cells, and were significantly higher in p73-and 14-3-3sigma-transfected H1299 cells than in p73-transfected H1299 cells (P<0.01). The number of colonies was fewer in p73-transfected MDA-MB-436 cells than in control MDA-MB-436 cells, and the colonies were significantly smaller in p73-and 14-3-3sigma-transfected H1299 cells than in p73-transfected H1299 cells (P<0.01). 14-3-3sigma can enhance the transcriptional activity of p73 in a dose-dependent manner.
    Ai zheng = Aizheng = Chinese journal of cancer 05/2007; 26(5):489-93.