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Liu S.-Y.,Guangdong Medical College | Liu S.-Y.,Shenzhen Nanshan Center for Chronic Disease Control | Wang W.,The First Hospital of Harbin | Cai Z.-Y.,Guangdong Medical College | And 5 more authors.
CNS Neuroscience and Therapeutics | Year: 2013

Aim: Alzheimer's disease (AD) is a multifactor disease that has been reported to have a close association with endoplasmic reticulum (ER) stress response. In the response, the regulator factor human X-box-binding protein 1 (XBP1) has been shown to facilitate the refolding and degradation of misfolded proteins, prevent neurotoxicity of amyloid-beta (Aβ) and tau, and play an important role in the survival of neurons. The aim in the study was to analyze the potential association between the -116C/G polymorphism of XBP1 and the risk of AD. Methods: The association between -116C/G polymorphism of XBP1 promoter and possible risk of AD was assessed among 276 patients with AD and 254 matched healthy individuals in a case-control study. Results: Overall, there was a significantly statistical difference in genotype (P = 0.0354) and allele frequencies (P = 0.0150, OR = 1.3642, 95% CI = 1.0618-1.7528) between the AD subjects and control subjects, showing that the -116C/G polymorphism of XBP1 might lead to increased susceptibility for AD in a Chinese Han population. In addition, the -116CG and -116GG genotypes were significantly associated with increased AD risk in female (P = 0.0217) and in subjects with APOE j{cyrillic, ukrainian}4 (-) (P = 0.0070) in stratified analyses, and the -116CC genotype was significantly associated with fast cognitive deterioration in the AD patients (P = 0.0270). Conclusion: The study supports a role for the -116C/G polymorphism of XBP1 gene in the pathogenesis of AD, and further studies with a larger sample size and detailed data should be performed in other populations. © 2013 Blackwell Publishing Ltd. Source


Yang S.,Harbin Medical University | Wang L.,The First Hospital of Harbin | Kong Q.,The First Hospital of Harbin
Cell Biochemistry and Biophysics | Year: 2014

Focal adhesion kinase (FAK), a nonreceptor tyrosine kinase protein, acts as an early modulator of integrin signaling cascade, regulating basic cellular functions. In transformed cells, unopposed FAK signaling has been considered to promote tumor growth, progression, and metastasis. The aim of this study was to assess the role of FAK in rat osteosarcoma OSR-6 cells. OSR-6 cells were transfected with PGPU6/GFP/shNC (shNC), and PGPU6/GFP/FAK-2434 (shRNA-2434), separately. Expression of FAK was detected by Real-time PCR and Western blots. MTT assay was used to examine changes in cell proliferation. Cell apoptosis was analyzed by flow cytometry. The expression of caspase-3,-7,-9 was measured by Western blots. The expression of FAK in OSR-6 cells significantly decreased in shRNA-2434 group in contrast to the control group (P < 0.01). Cell proliferation was inhibited by shRNA-2434 and shRNA-2434+ cisplatin, and the effects were clearly enhanced when cells were treated with anticancer agents. The level of cell apoptosis in shRNA-2434 and shRNA-2434+ cisplatin group was higher than that in the control group (P < 0.01). The current data support evidence that down-regulation of FAK could induce rat osteosarcoma cells (OSR-6) apoptosis through the caspase-dependent cell death pathway. Inhibition of the kinases may be important for therapies designed to enhance the apoptosis in osteosarcoma. © 2014, Springer Science+Business Media New York. Source


Wu Y.,Harbin Medical University | Ma Y.,Harbin Medical University | Xu Z.,Harbin Medical University | Wang D.,Harbin Medical University | And 9 more authors.
Cancer Letters | Year: 2014

The transition metal vanadium is widely distributed in the environment and exhibits various biological and physiological effects in the human body. As a well known vanadium compound, sodium orthovanadate (SOV) has shown promising antineoplastic activity in several human cancers. However, the effects of SOV on liver cancer are still unknown. In this study, for the first time, we showed that SOV could effectively suppress proliferation, induce G2/M cell cycle arrest and apoptosis, and diminish the mitochondrial membrane potential (MMP) of HCC cells in vitro. In addition, our in vitro results were recapitulated in vivo, showing that SOV exhibited a dose-dependent inhibition of growth of human HCC in an orthotopic model, evidenced by the reduction in tumor size, proliferation index and microvessel density, and increase in cell apoptosis. Most important, we found that SOV could inhibit autophagy in HCC cells in vitro and in vivo, which plays a prodeath role. Thus, our findings suggest that SOV could effectively suppress the growth of human HCC through the regulations of proliferation, cell cycle, apoptosis and autophagy, and thus may act as a potential therapeutic agent in HCC treatment. © 2014 Elsevier Ireland Ltd. Source


Zhao B.,Harbin Medical University | Ma Y.,Harbin Medical University | Xu Z.,Harbin Medical University | Wang J.,Harbin Medical University | And 8 more authors.
Cancer Letters | Year: 2014

The present study aimed to investigate the anti-cancer effects of hydroxytyrosol (HT) in human hepatocellular carcinoma (HCC) cells. Our results show that HT could inhibit proliferation, induce G2/M cell cycle arrest and apoptosis in human HCC cells. Mechanically, we found that HT could suppress the activation of AKT and nuclear factor-kappa B (NF-κB) pathways. HT also significantly inhibited the tumor growth, angiogenesis and the activation of AKT and NF-κB pathways in an orthotopic model of human HCC in vivo. These data suggest that HT may be a promising candidate agent for the treatment of HCC. © 2014 Elsevier Ireland Ltd. Source


Wang J.,Capital Medical University | Ning R.,The First Hospital of Harbin | Wang Y.,Capital Medical University
Journal of Stroke and Cerebrovascular Diseases | Year: 2016

Background: Despite being an important cause of death and functional disability, acute cerebral infarction (ACI) lacks accurate and easy tools to predict the outcome of patients beyond clinical variables such as age and stroke severity. Methods: To investigate if plasma D-dimer level can be used as such a prognostic biomarker for ACI, so as to better guide patients' management, we studied the association between plasma D-dimer and the functional recovery of 1173 ACI patients. The patients were divided into 2 groups according to modified Rankin Scale (mRS) scores or National Institutes of Health Stroke Scale (NIHSS) scores evaluated on the 30th day after onset. Results: We observed that plasma D-dimer level correlated significantly with the prognosis of ACI evaluated based on both mRS scores (389.68 ± 32.06 μg/L for poor prognosis versus 377.70 ± 32.68 μg/L for good prognosis, P < .001) and NIHSS scores (387.01 ± 30.60 μg/L for poor prognosis versus 375.23 ± 30.66 μg/L for good prognosis, P < .01). Logistic analysis confirmed that higher D-dimer level was a risk factor for poor prognosis (mRS: odds ratio [OR], 1.604; 95% confidence interval [CI], 1.360-1.892; P < .001; NIHSS: OR, 1.733; 95% CI, 1.461-2.056; P < .01), after adjusted for age, gender, hypertension, diabetes, smoking, and hyperlipidemia. Conclusion: Our results show that plasma D-dimer level is a promising prognosis biomarker for ACI. © 2016. Source

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