Huaiyin Hospital of Huaian City
Huaiyin Hospital of Huaian City
PubMed | Huaiyin Hospital of Huaian city, Shanghai JiaoTong University and The 82nd Hospital of the Peoples Liberation Army
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2016
Several aberrant microRNAs (miRNAs or miRs) have been implicated in esophageal cancer(EC), which is widely prevalent in China. However, their role in EC tumorigenesis has not yet been fully elucidated. In the present study, we determined that miR1 was downregulated in esophageal squamous cell carcinoma(ESCC) tissues compared with adjacent non-neoplastic tissues using RT-qPCR, and confirmed this using an ESCC cell line. Using a nude mouse xenograft model, we confirmed that the re-expression of miR1 significantly inhibited ESCC tumor growth. A tetrazolium assay and a trypan blue exclusion assay revealed that miR1 suppressed ESCC cell proliferation and increased apoptosis, whereas the silencing of miR1 promoted cell proliferation and decreased apoptosis, suggesting that miR1 is a novel tumor suppressor. To elucidate the molecular mechanisms of action of miR1 in ESCC, we investigated putative targets using bioinformatics tools. MET, cyclinD1 and cyclin-dependent kinase4(CDK4), which are involved in the hepatocyte growth factor (HGF)/MET signaling pathway, were found to be targets of miR1. miR1 expression inversely correlated with MET, cyclinD1 and CDK4 expression in ESCC cells. miR1 directly targeted MET, cyclinD1 and CDK4, suppressing ESCC cell growth. The newly identified miR1/MET/cyclinD1/CDK4 axis provides new insight into the molecular mechanisms of ESCC pathogenesis and indicates a novel strategy for the diagnosis and treatment of ESCC.
PubMed | Huaiyin Hospital of huaian city, Huaian Maternity and Child Health Care Hospital, Nanjing Maternity and Child Health Care Hospital, Xuzhou Medical University and Nanjing Medical University
Type: | Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | Year: 2016
MicroRNAs act as posttranscriptional regulators of gene expression in many biological processes, which played a vital role in regulation cancer cells epithelial-to-mesenchymal transition and metastasis. The deregulation of miR-381 has been identified in breast cancer. However, the role and mechanism of miR-381 in breast cancer have not been completely unexplored.Total RNA was extracted from the tissues of 27 patients with breast cancer and two breast cancer cell lines, respectively. The expression levels of miR-381 were examined by quantitative real-time PCR. The stable overexpress or silence miR-381 expression cells lines and control cells line were constructed by lentivirus infection. Subsequently, cell proliferation, cell migration, invasion assay and western blot assay were performed to detect the biological functions of miR-381 in vitro. Moreover, a luciferase reporter assay was conducted to confirm target associations.In this study, we validated the lower expression of miR-381 in breast cancer tissues than their adjacent non-neoplastic tissues in 27 breast cancer patients. The result also showed that miR-381 was lowly expressed in breast cancer cell lines MCF-7 and MDA-MB-231 than human epithelial cell line MCF-10A. The miR-381 expression was significantly up-regulated under exogenous miRNA-381 treatment in MCF-7 and MDA-MB-231 cells analyzed by quantitative real-time PCR. The results also indicated that an inverse correlation existed between miR-381 expression level and breast cancer cell proliferation, epithelial-to-mesenchymal transition and metastasis. Furthermore, miR-381 was predicted as a regulatory miRNA of CXCR4 in breast cancer, and the data analysis revealed that there was a negatively relationship between miR-381 and CXCR4 expression in breast cancer tissues from the patients. miR-381 played an important role in breast cancer cells proliferation, epithelial-to-mesenchymal transition and metastasis by targeting CXCR4.This present study revealed that miR-381 might be considered as a novel therapeutic target for breast cancer treatment.
Yang W.,Nanjing Medical University |
Tian R.,Air Force General Hospital of PLA |
Xue T.,Huaiyin Hospital Of Huaian City
Tumor Biology | Year: 2015
We evaluated whether degrees of dysplasia may be consistently accessed in an automatic fashion, using different kinds of non-melanoma skin cancer (NMSC) as a validatory model. Namely, we compared Bowen disease, actinic keratosis, basal cell carcinoma, low-grade squamous cell carcinoma, and invasive squamous cell carcinoma. We hypothesized that characterizing the shape of nuclei may be important to consistently diagnose the aggressiveness of a skin tumor. While basal cell carcinoma is comparatively relatively benign, management of squamous cell carcinoma is controversial because of its potential to recur and intraoperative dilemma regarding choice of the margin or the depth for the excision. We provide evidence here that progressive nuclear dysplasia may be automatically estimated through the thresholded images of skin cancer and quantitative parameters estimated to provide a quasi-quantitative data, which can thenceforth guide the management of the particular cancer. For circularity, averaging more than 2500 nuclei in each group estimated the means ± SD as 0.8 ± 0.007 vs. 0.78 ± 0.0063 vs. 0.42 ± 0.014 vs. 0.63 ± 0.02 vs. 0.51 ± 0.02 (F = 318063.56, p < 0.0001, one-way analyses of variance). The mean aspect ratios were (means ± SD) 0.97 ± 0.0014 vs. 0.95 ± 0.002 vs. 0.38 ± 0.018 vs. 0.84 ± 0.0035 vs. 0.74 ± 0.019 (F = 1022631.931, p < 0.0001, one-way analyses of variance). The Feret diameters averaged over 2500 nuclei in each group were the following: 1 ± 0.0001 vs. 0.9 ± 0.002 vs. 5 ± 0.031 vs. 1.5 ± 0.01 vs. 1.9 ± 0.004 (F = 33105614.194, p < 0.0001, one-way analyses of variance). Multivariate analyses of composite parameters potentially detect aggressive variants of squamous cell carcinoma as the most dysplastic form, in comparison to locally occurring squamous cell carcinoma and basal cell carcinoma, or benign skin lesions. © 2015, International Society of Oncology and BioMarkers (ISOBM).
PubMed | Huaiyin hospital of Huaian city, Huaian First Peoples Hospital and Soochow University of China
Type: Journal Article | Journal: PloS one | Year: 2016
Osteoporosis is one of the most prevalent skeletal system diseases. It is characterized by a decrease in bone mass and microarchitectural changes in bone tissue that lead to an attenuation of bone resistance and susceptibility to fracture. Vertebral fracture is by far the most prevalent osteoporotic fracture. In the musculoskeletal system, osteoblasts, originated from bone marrow stromal cells (BMSC), are responsible for osteoid synthesis and mineralization. In osteoporosis, BMSC osteogenic differentiation is defective. However, to date, what leads to the defective BMSC osteogenesis in osteoporosis remains an open question. In the current study, we made attempts to answer this question. A mouse model of glucocorticoid-induced osteoporosis (GIO) was established and BMSC were isolated from vertebral body. The impairment of osteogenesis was observed in BMSC of osteoporotic vertebral body. The expression profiles of thirty-six factors, which play important roles in bone metabolisms, were compared through antibody array between normal and osteoporotic BMSC. Significantly higher secretion level of IL-6 was observed in osteoporotic BMSCs compared with normal control. We provided evidences that IL-6 over-secretion impaired osteogenesis of osteoporotic BMSC. Further, it was observed that -catenin activity was inhibited in response to IL-6 over-secretion. More importantly, in vivo administration of IL-6 neutralizing antibody was found to be helpful to rescue the osteoporotic phenotype of mouse vertebral body. Our study provides a deeper insight into the pathophysiology of osteoporosis and identifies IL-6 as a promising target for osteoporosis therapy.
Yuan Q.,Huaiyin Hospital of Huaian City |
Wang M.,Nanjing Medical University |
Zhang Z.,Nanjing Medical University |
Zhang W.,Nanjing Medical University
Molecular Biology Reports | Year: 2012
Inflammatory factors may promote carcinogenesis. Macrophage migration inhibitory factor (MIF), which is derived from T-cell, known as a member of the transforming growth factor-β (TGF-β) superfamily, plays an important role in the pro-and anti-inflammatory response to infection and in the etiology of bladder cancer. We hypothesized that MIF-173 locus polymorphism might contribute to genetic susceptibility to bladder cancer. In a hospital-based case-control study of 325 patients with bladder cancer and 345 cancer-free controls frequencymatched by age, sex, smoking status, and alcohol use, we genotyped the MIF polymorphism and analyzed immunohistochemical stained operational bladder cancer tissue sections for MIF. We found that individuals with GC/CC genotype had a significantly decreased risk of bladder cancer (adjusted OR = 0.57, 95% CI, 0.41-0.79) than those with GG genotype. In the stratification analysis, we found that the decreased risk was more pronounced among older subjects (adjusted OR = 0.56, 95% CI, 0.39-0.81), men (0.47, 0.33-0.68), smokers (0.54, 0.35-0.85), and ever-drinkers (0.44, 0.27-0.71). The percentage of positive staining in the cytoplasm and nucleus in the normal and bladder cancer with CC/GC genotype tissues was higher than that of GG genotype bladder cancer tissue(39.1% vs. 75.0% in strong staining for GG and GC/CC genotypes, respectively, P = 0.028). In conclusion, MIF -173G[C polymorphism may play a role in the etiology of bladder cancer in southern Chinese population. Large studies are warranted to validate our findings © Springer Science+Business Media B.V. 2011.
PubMed | Huaiyin Hospital of Huaian City and Nanjing Medical University
Type: | Journal: Medical science monitor : international medical journal of experimental and clinical research | Year: 2016
BACKGROUND Single-nucleotide polymorphisms (SNPs) located at lncRNA may affect the stability and splicing processes of mRNA formation, which result in the alteration of its interacting partners. The SNP rs755622 within exon of antisense lncRNA MIF- AS and promoter of MIF was implicated in renal disease risk. MATERIAL AND METHODS In this case-control study, we genotyped the SNP rs755622 in 230 patients diagnosed with nephrolithiasis and 250 controls in a Chinese population. RESULTS We found that the rs755622 CG and CC genotypes had a significantly increased nephrolithiasis risk (adjusted OR=1.52, 95% CI=1.03-2.25; OR=2.63, 95% CI=1.21-5.72, P=0.015), compared with GG genotype in the additive model. The rs755622 C carriers (GC/CC) had an adjusted OR (95% CI) of 1.65 (1.14-2.39, P=0.016), compared with the GG genotype in the dominant model. This hazardous effect was more pronounced in subgroup age >46, BMI >24, hypertension, ever smoking, and ever drinking subjects. Moreover, we found that rs755622 could modulate the function of MIF-AS by influencing its folding. CONCLUSIONS These results indicate that the MIF-AS rs755622 polymorphism may have a crucial role in the development of nephrolithiasis.
Yin H.-Y.,Huaiyin Hospital of Huaian City |
Wei J.,Nan Chen Set Branch of Huaiyin Hospital of Huaian City
Journal of Practical Oncology | Year: 2014
Objective: To investigate the differential gene expression profile of paclitaxel (taxol)-resistant human lung adenocarcinoma A549 cells.Methods: The effect of taxol on human lung adenocarcinoma A549 cells and drug-resistant A549/taxol cells was determined by Kaplan-Meier survival curve. The differential gene expression of A549 and A549/taxol cells was examined by microarray assay.Results: The Kaplan-Meier curve showed that mice injected with A549 cells lived 25 days longer than the group injected with A549/taxol cells with the same taxol-based program(P<0.01). Genome-wide expression in these cells revealed that overall 163 and 115 genes were upregulated or downregulated >3 folds, respectively, in A549/taxol cells.Conclusion: The difference in genomic expression may be one of the mechanisms of taxol resistance in A549/taxol cells.
Li H.,Second Peoples Hospital of Huaian |
Qiao Y.,Second Peoples Hospital of Huaian |
Shen Y.,Second Peoples Hospital of Huaian |
Fei Q.,Second Peoples Hospital of Huaian |
And 2 more authors.
Cancer Research and Clinic | Year: 2016
Objective: To study the correlation between microRNA (miRNA) polymorphism and the risk and clinical prognosis of acute radiation esophagitis in patients with esophageal neoplasms. Methods: 256 patients with acute radiation esophagitis during radiotherapy were chosen as the experimental group, and 256 patients matched by age and sex without acute radiation esophagitis during radiotherapy were chosen as the control group. The polymorphism types of miRNA-146a (rs29lOl64) were determined by Taqman gene typing technology of ABI7900HT. The genotype distribution of miRNA-146a rs2910164 polymorphism in the experimental and control groups was analyzed. Logistic regression was performed to estimate the odds ratio (OR) and 95 % confidence interval (95 % CI). Results: The genotype frequencies of CC, GG and CG at miRNA-146a polymorphic site rs2910164 in the experiment and control group were 20.70 % (53/256) and 33.20 % (85/256), 45.32 % (116/256) and 40.63 % (104/256), 33.98 % (87/256) and 26.17 % (67/256), respectively. There was a statistically significant difference between two groups (all P < 0.05). Compared with gene type CC, the OR values of acute radiation esophagitis in patients with gene type GC and GG were 0.654 and 0.627, respectively (P < 0.05), indicating that they had a low risk. The negative effect rates in patients with gene type GG, CG and CC were 7.69 % (8/104), 19.40 % (13/67) and 41.18 % (35/85), respectively. There was a statistically significant difference in the clinical prognosis among these genotypes (P < 0.05). Conclusion: Gene type CC at miRNA-146a polymorphic site rs2910164 can increase the risk of acute radiation esophagitis and decrease the clinical prognosis in patients with esophageal neoplasms. © Copyright 2016 by the Chinese Medical Association.
Lu D.-Q.,Huaiyin Hospital Of Huaian City |
Wang X.-F.,Huaiyin Hospital Of Huaian City
World Chinese Journal of Digestology | Year: 2015
Caroli disease is a rare congenital disease characterized by cystic dilatation of the intrahepatic bile ducts. Caroli disease with hepatitis B is even rarer. For hepatitis B patients, antiviral therapy is effective. For patients with recurrent bilirubin abnormality, clinicians should raise their awareness to rule out Caroli disease. © 2015 Baishideng Publishing Group Inc. All rights reserved.
Pan X.-F.,Huaiyin Hospital of Huaian City |
Yin H.-Y.,Huaiyin Hospital of Huaian City
Journal of Practical Oncology | Year: 2014
Objective: To investigate the effect of silver nanoparticles on the proliferation of human lung carcinoma A549 cells and its mechanism. Methods: Cultured A549 cells were treated with different concentrations of silver nanoparticles in vitro. The morphological change of A549 cells was observed by microscopy. Cell proliferation was determined by MTT assay. Cell cycle was examined by flow cytometry and the expression of p21, p53, Bcl-2 and caspase-3 proteins was detected by Western blot and immunohistochemistry. Results: Compared with control group, the inhibition of A549 cells was significantly increased as the concentration of silver nanoparticles increased[IC50=(74.23±4.17)mg/L]. After silver nanoparticle treatment, cell cycle was arrested in G2/M phase; the expression of p21, p53 and caspase-3 was increased and the expression of Bcl-2 was decreased. Conclusion: Silver nanoparticles can inhibit the proliferation of A549 cells, which is associated with the blockage in G2/M phase, the up-regulation of p21, p53 and caspase-3 expression, and the down-regulation of Bcl-2 expression.