Chen P.,Qufu Normal University |
Lao H.,Binzhou Central Hospital |
Qu F.,Qufu Normal University |
You J.,Qufu Normal University |
And 2 more authors.
New Journal of Chemistry | Year: 2017
Utilizing the switch effect of Bi3+, a sensitive turn off-on ratiometric fluorescent sensor based on dual-emission carbon-dots has been developed for captopril in aqueous solutions. © The Royal Society of Chemistry and the Centre National de la Recherche Scientifique.
Bai W.,Nanjing Medical University |
Bai J.,Nanjing Medical University |
Li Y.,Binzhou Central Hospital |
Tian D.,Binzhou Central Hospital |
Shi R.,Nanjing Medical University
Biochemical and Biophysical Research Communications | Year: 2017
Many autophagy-related genes, to our knowledge, have been identified as Crohn's disease (CD) polymorphic sites by genomic wide studies. As a novel member of the microtubule-associated protein 1 (MAP1) family, MAP1S is a microtubule-binding proteins involved in autophagy. However, its expression and potential functions in CD have not been understood. For the first time, we discovered the up-regulated MAP1S and autophagy level (indicated by LC3-Ⅱ/LC3-Ⅰ) in inflamed epithelium among CD patients. Similarly, in TNBS-induced murine colitis model, MAP1S expression was obviously increased. Meanwhile, we found the co-location of MAP1S and active-caspase 3 which acted as “apoptotic executor” which might indicate the basis of their co-efficient. At the cellular level, MAP1S silencing inhibited starvation-induced over-expression of active-caspase 3 partially via Wnt/β-catenin signaling activation in HCT-116 cells. Finally, we demonstrated that IWP-2, an inhibitor of the Wnt/β-catenin signaling, reversed the down-regulation of active-caspase 3 induced by MAP1S siRNA in HCT-116 cells. Taken together, our results suggested that MAP1S were up-regulated among CD patients and MAP1S-related autophagy inhibits apoptosis of intestinal epithelial cells (IECs) through Wnt/β-catenin signaling pathway which might play a vital role in the protection of intestinal mucosal barrier and inhibition the progression of CD. © 2017 Elsevier Inc.
PubMed | Binzhou Central Hospital and Shanghai University
Type: Journal Article | Journal: Digestive diseases and sciences | Year: 2016
That obesity leads to gastroesophageal reflux is a widespread notion. However, scientific evidence for this association is limited, with no rigorous epidemiological approach conducted to address this question. This study examined the relationship between body mass index (BMI) and gastroesophageal reflux symptoms in a large population-representative sample from China.We performed a cross-sectional study in an age- and gender-stratified random sample of the population of five central regions in China. Participants aged 18-80years completed a general information questionnaire and a Chinese version of the Reflux Disease Questionnaire. The zero-inflated Poisson regression model estimated the relationship between body mass index and gastroesophageal reflux symptoms.Overall, 16,091 (89.4%) of the 18,000 eligible participants responded. 638 (3.97%) and 1738 (10.81%) experienced at least weekly heartburn and weekly acid regurgitation, respectively. After adjusting for potential risk factors in the zero-inflated part, the frequency [odds ratio (OR) 0.66, 95% confidence interval (95% CI) 0.50-0.86, p=0.002] and severity (OR 0.66, 95% CI 0.50-088, p=0.004) of heartburn in obese participants were statistically significant compared to those in normal participants. In the Poisson part, the frequency of acid regurgitation, overweight (OR 1.10, 95% CI 1.01-1.21, p=0.038) and obesity (OR 1.19, 95% CI 1.04-1.37, p=0.013) were statistically significant. BMI was strongly and positively related to the frequency and severity of gastroesophageal reflux symptoms. Additionally, gender exerted strong specific effects on the relationship between BMI and gastroesophageal reflux symptoms.The severity and frequency of heartburn were positively correlated with obesity. This relationship was presented distinct in male participants only.
Wang P.-Y.,Binzhou Medical University |
Wang P.-Y.,Shandong University |
Xie S.-Y.,Binzhou Medical University |
Hao Q.,Binzhou Central Hospital |
And 2 more authors.
International Journal of Tuberculosis and Lung Disease | Year: 2012
BACKGROUND AND OBJECTIVE: Although a series of studies have evaluated the potential association between N-acetyltransferase 2 (NAT2) polymorphisms and the risk of anti-tuberculosis drug-induced liver injury (ATLI), the results have generally been controversial and inadequate, mainly due to limited power. The present metaanalysis sought to resolve this problem. DESIGN: PubMed, Embase and Web of Science were searched using the following key words: 'N-acetyltransferase 2' or 'NAT2' and 'polymorphism' and 'tuberculosis'or 'TB' and 'hepatotoxicity' or 'liver injury'. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were summarised in forest plots and set out in a table. RESULTS: A total of 14 studies, comprising 474 cases and 1446 controls, were included in the meta-analysis. A significant association was observed between NAT2 slow acetylators and the risk of ATLI. The OR for NAT2 slow acetylators compared with rapid acetylators was 4.697 (95%CI 3.291-6.705, P < 0.001). Subgroup analyses indicate that both Asian and non-Asian cases with slow acetylators develop ATLI more frequently, which is similar to patients with slow acetylators receiving firstline combination treatment. On comparing NAT2 intermediate acetylators with rapid acetylators, the OR for ATLI was 1.261 (95%CI 0.928-1.712, P = 0.138). CONCLUSIONS: This meta-analysis showed that tuberculosis patients with slow acetylators had a higher risk of ATLI than other acetylators. Screening of patients for the NAT2 genetic polymorphisms will be useful for the clinical prediction and prevention of ATLI. © 2012 The Union.
Shi H.-Z.,Binzhou Central Hospital |
Ren P.,Binzhou Central Hospital |
Lu Q.-J.,Binzhou Central Hospital |
Niedrgethmnn M.,University of Mannheim |
Wu G.-Y.,Xiamen University
Asian Pacific Journal of Cancer Prevention | Year: 2012
Introduction: Up to present, EGF 61*A/G, TGF-ß1-509*T/C and TNF-a-308*A/G gene polymorphisms have been analysed in other cancer entities than hepatocellular carcinoma (HCC). We here investigated the frequency of these gene polymorphisms among HCC patients. Materials and Methods: A total of 73 HCC patients and 117 cancer-free healthy people were recruited at the Surgical Department of Zhongshan Hospital. Genomic DNA was isolated from peripheral blood and gene polymorphisms were analyzed by PCR-RFLP. Results: The distribution of EGF 61*G/G homozygotes among HCC patients was more frequent than that in the control group (24.7% vs 11.1%, OR=2.618, 95%CI=1.195-5.738). In parallel, the frequency of the "G" allele in the HCC patient group was also higher than that in the control group (45.9% vs 33.3%, OR= 1.696, 95%CI=1.110-2.592). No difference could be found for the TGF-ß1-509 and TNF-a-308 genotypes. Conclusion: EGF 61*G/G genotype and G allele are significantly increased among patients with HCC. TGF-ß1-509*T/C and TNF-a-308*A/G gene polymorphisms are not related to this cancer entity.
Xiong Y.,Xiamen University |
Lu Q.-J.,Binzhou Central Hospital |
Zhao J.,Shandong University |
Wu G.-Y.,Xiamen University
Asian Pacific Journal of Cancer Prevention | Year: 2012
Recently, population-based studies of type 2 diabetes patients have provided evidence that metformin treatment is associated with a reduced cancer incidence and mortality, but its mode of action remains unclear. Here we report effects of metformin on hepatocellular carcinoma (HCC) Hep-G2 cells and details of molecular mechanisms of metformin activity. Our research indicates that metformin displays anticancer activity against HCC through inhibition of the mTOR translational pathway in an AMPK-independent manner, leading to G1 arrest in the cell-cycle and subsequent cell apoptosis through the mitochondrion-dependent pathway. Furthermore, we showed that metformin strongly attenuated colony formation and dramatically inhibited Hep-G2 tumor growth in vivo. In conclusion, our studies suggested that metformin might have potential as a cytotoxic drug in the prevention and treatment of HCC.
Shen T.,Shandong University |
Li W.,Binzhou Central Hospital |
Wang Y.-Y.,Shandong University |
Zhong Q.-Q.,Shandong University of Traditional Chinese Medicine |
And 4 more authors.
Archives of Pharmacal Research | Year: 2014
In our cell based screening of antitumor ingredients from plants, the EtOH extract of Garcinia bracteata displayed antiproliferative effect against human lung adenocarcinoma A549 cells, human breast cancer MCF-7 cells, and human prostate cancer PC3 cells. Phytochemical investigation of this active extract produced nine ingredients, and their structures were established by analysis of MS and NMR spectra. Antiproliferative evaluation of isolated ingredients on A549, MCF-7 and PC3 cells indicated that a xanthone named isobractatin (1) exhibited potent antiproliferative activity against the above three human cancer cell lines with IC50 values ranging from 2.90 to 4.15 μM. Treatment of PC3 cells with 1 led to an enhancement of the cell apoptosis, and arrested cell cycle in the G0/G1 phase. The G0/G1 phase cycle-related proteins analysis showed that the expressions of cyclins D1 and E were reduced by 1, whereas the protein level of cyclin dependent kinase (CDK) inhibitor P21 was induced. Additionally, 1 enhanced PC3 cell apoptosis by activations of Bax, caspases 3 and 9, and by inhibition of Bcl-2. Our combined data illustrated that isobractatin (1) was the antiproliferative ingredient of G. bracteata against three human cancer cell lines, which exerted its antiproliferatrive effect via cell cycle arrest and induction of apoptosis. © 2013 The Pharmaceutical Society of Korea.
Lv H.,Qingdao University |
Gao G.,Binzhou Central Hospital |
Zhang L.,Peoples Hospital of Gaomi |
Sun Y.,Qingdao University
Molecular Medicine Reports | Year: 2015
Polo-like kinase 3 (Plk3) is a member of the Plk family. It is dysregulated in certain types of cancer, including colorectal and pancreatic cancer. However, the expression status and biological function of Plk3 in osteosarcoma (OS) remain poorly understood. Following evaluation of the role of Plk3 in OS, the present study indicates that Plk3 is downregulated in OS cell lines and tissues, and increased expression levels of Plk3 are associated with improved rates of overall survival of patients. In addition, to investigate the role of Plk3 in cell proliferation and tumorigenicity in vitro, two recombinant lentiviruses expressing Plk3 short hairpin RNA, as well as a recombinant plasmid carrying Plk3, were developed and transfected into Saos-2 and U2OS cells, respectively. Cell cycle analysis by flow cytometry demonstrated the influence of Plk3 on the arrest of cell cycle progression at the G1 phase. Following knock down of Plk3, the growth and colony formation of Saos-2 cells increased significantly, whereas the overexpression of Plk3 resulted in the opposite trend. Furthermore, a 5-ethynyl-2'-deoxyuridine assay, using U2OS cell lines, indicated the same tendency. The in vivo interaction between Plk3 and p21 in Saos-2 cells was detected and the protein level of p21 was observed to be consistent with that of Plk3. These results imply that Plk3 is involved in the inhibition of cell proliferation and tumorigenesis, which may occur via interactions with p21, thus, Plk3 may be considered as a potential candidate for targeted therapy of OS.
PubMed | Binzhou Central Hospital, The Peoples Hospital of Gaomi and Qingdao University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015
Pololike kinase 3 (Plk3) is a member of the Plk family. It is dysregulated in certain types of cancer, including colorectal and pancreatic cancer. However, the expression status and biological function of Plk3 in osteosarcoma (OS) remain poorly understood. Following evaluation of the role of Plk3 in OS, the present study indicates that Plk3 is downregulated in OS cell lines and tissues, and increased expression levels of Plk3 are associated with improved rates of overall survival of patients. In addition, to investigate the role of Plk3 in cell proliferation and tumorigenicity in vitro, two recombinant lentiviruses expressing Plk3 short hairpin RNA, as well as a recombinant plasmid carrying Plk3, were developed and transfected into Saos2 and U2OS cells, respectively. Cell cycle analysis by flow cytometry demonstrated the influence of Plk3 on the arrest of cell cycle progression at the G1 phase. Following knock down of Plk3, the growth and colony formation of Saos2 cells increased significantly, whereas the overexpression of Plk3 resulted in the opposite trend. Furthermore, a 5ethynyl2deoxyuridine assay, using U2OS cell lines, indicated the same tendency. The in vivo interaction between Plk3 and p21 in Saos2 cells was detected and the protein level of p21 was observed to be consistent with that of Plk3. These results imply that Plk3 is involved in the inhibition of cell proliferation and tumorigenesis, which may occur via interactions with p21, thus, Plk3 may be considered as a potential candidate for targeted therapy of OS.
PubMed | Binzhou Central Hospital
Type: Journal Article | Journal: European review for medical and pharmacological sciences | Year: 2017
MicroRNAs (miRs) regulate the proliferation and metastasis of numerous cancer cell types. This study aimed to reveal the role of microRNA-542-3p (miR-542-3p) in breast cancer (BC) cell proliferation and its potential mechanisms.MiR-542-3p expression was detected by reverse transcription-polymerase chain reaction (RT-PCR) and sphingosine-1-phosphate receptor 1(S1PR1) protein expression was measured by Western blotting. TargetScan was used to predict the downstream target genes of miR-542-3p, which were confirmed by luciferase and RNA immunoprecipitation assays. Biological functions of miR-542-3p and S1PR1 were analyzed using CKK-8, colony formation, migration, and invasion.It was demonstrated that the expression of miR-542-3p was downregulated in BC tissues and cell lines. We also showed that the expression of S1PR1 was upregulated in BC tissues and cell lines. Furthermore, we found that the expression level of miR-542-3p was negatively correlated with the expression level of S1PR1 in BC tissues. Over-expression of miR-542-3p inhibited BC cell proliferation, colony formation, migration and invasion. The dual luciferase reporter experiments showed that miR-542-3p regulated the expression of S1PR1 by combining with its 3UTR. Finally, we showed that down-expression of miR-542-3p inhibited BC cell proliferation, colony formation, migration and invasion.Our study provides the new insight that miR-542-3p inhibited colon cancer cells via targeting S1PR1, suggesting that miR-542-3p/S1PR1 can serve as a potential therapeutic target for BC.