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Li Z.,Shanghai University | Wang J.,Zhejiang Police College | Zhou T.,Hepatobiliary Surgery Center | Ye X.,Ningbo Institute of Medical science
Oncology Letters | Year: 2016

The aim of the present study was to establish a model of tumor cell growth and visualize HIF-1α overexpression in a nude mouse xenograft model of colorectal cancer (CRC). In the study, HIF-1α lentiviral vector and helper plasmid were co-transfected into 293T packaging cells using a liposome method, and the virus was collected following transfection and used to infect CRC SW480, SW620, LoVo and HCT116 cells. Puromycin was used for the selection and large-scale amplification of the stable HIF-1α expression of green fluorescent protein (GFP)-positive cells. HIF-1α-expressing cells were injected intraperitoneally into a nude mouse xenograft model, and resulting tumor nodules was separated and confirmed using an inverted fluorescence microscope. The results demonstrated that HIF-1α was not expressed in CRC cells in normoxic conditions. When treated with CoCl2, the expression of HIF-1α could be induced in all the cancer cell lines, except SW480. HIF-1α was highly expressed following infection with lentiviral particles. Stable expression of HIF-1α promoted migration in the SW480 cells. Following intraperitoneal injection of nude mice with SW480-HIF-1α, a significant number of tumor nodules formed in the intestinal wall compared with the controls (P<0.05). The successful construction of the dual expression HIF-1α and GFP visualization xenograft model provides a good foundation for the screening of HIF-1α-related functions and for investigating the therapeutic potential of drugs that target HIF-1α. © 2016, Spandidos Publications. All rights reserved. Source


Gao Y.-F.,Weifang Peoples Hospital | Wei X.-N.,China Pharmaceutical University | Ye X.-L.,Ningbo Institute of Medical science | Weng G.-B.,Second Street | And 3 more authors.
Molecular Medicine Reports | Year: 2015

Stoppin (L1) is a newly identified anticancer peptide, which is a potent p53-MDM2/MDMX inhibitor. Due to its limitation in cell delivery efficiency, a new peptide delivery system was developed based on a nucleic acid-polypeptide-liposome complex and its stability and effectiveness in vitro was investigated. The nucleic acid-stoppin-liposome complex was prepared and characterization of the complex was conducted. The stability of the complex was evaluated by enzyme digestion. Following transfection of the A549 cells with the complex, detection of green fluorescent protein (GFP) and luciferase activity was conducted to evaluate transfection efficiency. In addition, the anticancer activity of the complex was determined by 3-(4,5-dimethyl-thiazolyl-2)-2,5 diphenyltetrazolium bromide assay and apoptosis was detected by flow cytometry. The results indicated that the particle size of the complex was 102±10 nm and the encapsulation rate was ∼100% when the ratio of liposome, L1 and plasmid was: 4 μl:1 μg:2 μg. The enzyme digestion experiment demonstrated that the complex was resistant to pancreatic and DNA enzyme degradation, indicating that the complex had biological stability. Cell transfection demonstrated that it had a mutual promotion effect on delivery, which could be confirmed by GFP fluorescence and luciferase assay. The cell-killing efficiency of this novel delivery system was three times higher than with stoppin alone at a low concentration. In conclusion, this novel stoppin peptide delivery system was stable. The nucleic acid-peptide-liposome complex can protect the internal component from the degradation of enzymes, promote entry of the peptide into the cells and enhance the anti-tumor activity of stoppin. Therefore, it is a promising approach for peptide delivery, which can be characterized and visualized using plasmids with GFP or luciferase. Source


Xu M.,Ningbo University | Ye X.,Ningbo Institute of Medical science | Zhao F.,Ningbo University | He Y.,Ningbo University | Chen L.,Chinese PLA General Hospital
ORL | Year: 2014

Aims: The aim of this study was to analyze the relationship between allergy and different subtypes of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods: A total of 83 patients with CRSwNP and 20 patients with nasal septum deviation (NSD) as controls were enrolled in our study. Nasal tissue was obtained from all subjects during surgery. Hematoxylin and eosin staining was performed and the CRSwNP cases were classified into eosinophilic nasal polyps (ENP) and noneosinophilic nasal polyps (nENP) cases according to the percent of eosinophils. The Allergy Screen test was used to detect total and specific immunoglobulin E (IgE) against 5 kinds of common inhalant allergens. Results: There were 28 (33.73%) patients with ENP and 55 with nENP. Total IgE levels were significantly increased in ENP compared with nENP patients. The IgE level was significantly correlated with the eosinophil count. According to the 5 kinds of common inhalant allergens, only ENP patients exhibited higher sensitivity to dust mites. Conclusion: Patients with ENP showed significantly higher IgE levels when compared with patients with nENP based on allergy. © 2015 S. Karger AG, Basel. Source


Wu T.,Zhejiang University | Xu Y.-H.,Shanghai JiaoTong University | Ye X.-L.,Ningbo Institute of Medical science
Tumor Biology | Year: 2013

There were many studies performed to assess the association between X-ray repair cross-complementing group 1 (XRCC1) Arg194Trp polymorphism and lung cancer risk in Chinese Han population, but contradictory results were reported. To provide a comprehensive and objective assessment of the association, a meta-analysis of all eligible case-control studies was carried out. After searching the databases and reading the abstracts, 12 case-control studies on the association between XRCC1 Arg194Trp polymorphism and lung cancer risk were finally included into this meta-analysis. Those 12 studies included a total of 4,385 cases and 4,545 controls. XRCC1 Arg194Trp polymorphism was associated with increased risk of lung cancer in Chinese Han population under three main models (allele contrast model, odds ratio (OR) = 1.12, 95 % confidence interval (CI) 1.00-1.26, P = 0.049; homozygote model, OR = 1.27, 95 % CI 1.09-1.48, P = 0.003; recessive model, OR = 1.26, 95 % CI 1.09-1.46, P = 0.003). However, there was no obvious association between XRCC1 Arg194Trp polymorphism and lung cancer risk under the dominant model (OR = 1.06, 95 % CI 0.98-1.16, P = 0.146). Sensitivity analysis suggested the stability and liability of this meta-analysis. Therefore, this meta-analysis suggests that XRCC1 Arg194Trp polymorphism is associated with increased risk of lung cancer in Chinese Han population. © 2013 International Society of Oncology and BioMarkers (ISOBM). Source


Che X.-H.,Ningbo Institute of Medical science | Che X.-H.,Yichun University | Chen C.-L.,Yichun University | Ye X.-L.,Ningbo Institute of Medical science | And 6 more authors.
Oncology Reports | Year: 2016

Inflammation is emerging as a new hallmark of cancer. Arachidonic acid (AA) metabolism, the family of cyclooxygenases (COXs) and lipoxygenase (LOX) play important roles in AA-related inflammatory cascades. In 94 colorectal cancer samples collected from the Han population, the immunohistochemical results indicated that 68% of the patients with colorectal cancer had a co-expression of both COX-2 and 5-LOX, while both displayed low expression in the matched normal tissues. In cell lines, three colorectal cancer cell lines exhibited high expression of COX-2 and 5-LOX. During stable silencing of the expression of COX-2 or 5-LOX in LoVo cancer cells, we found that downregulation of either COX-2 or 5-LOX significantly diminished the growth, migration and invasion of the colon cancer cells and specifically, downregulation of COX-2 could elicit upregulation of 5-LOX protein and vice versa. The above results suggested that the simultaneous blocking of COX-2 and 5-LOX activity may bring more potential benefits in managing the progression of colon cancer. Therefore, we sought to explore the effectiveness of a dual COX-2/5-LOX inhibitor darbufelone on the proliferation, migration, invasion and apoptosis of colon cancer cells, as well as the underlying mechanism of action. The results indicated that darbufelone significantly decreased the proliferative and invasive abilities of the colon cancer cells, in a dose-dependent manner. During the study of the related mechanisms, we found an upregulation of p27 and downregulation of cyclin D1 as well as CDK4 after darbufelone treatment, which indicated that darbufelone could arrest the cell cycle of LoVo cells at the G0/G1 phase. Furthermore, the activation of caspase-3 and -9, upregulation of Bax and downregulation of Bcl-2 demonstrated the occurrence of apoptosis by darbufelone. Finally, darbufelone also prevented the migration and invasion of LoVo cells, which may be ascribed to the upregulation of E-cadherin and ZO-1. In summary, our data suggest that the inhibition of both COX-2/5-LOX may be an effective therapeutic approach for colon cancer management, particularly for those patients with high expression of COX-2/5-LOX. Source

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