Tianjin Huan Hu Hospital

Tianjin, China

Tianjin Huan Hu Hospital

Tianjin, China
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Shu C.,Nankai University | Wang J.,Nankai University | Wang J.,Tianjin Huan Hu Hospital
Meta Gene | Year: 2017

A FGFR4 Gly388Arg polymorphism (rs351855) which caused the substitution of arginine for glycine in the transmembrane domain of the receptor, was reported to increase cancer risk or not. According to this reason, a meta analysis was made, including a total of 4767 cases and 5817 controls. The results showed that FGFR4 Gly388Arg polymorphism (rs351855) might be an cancer risk factor for majority Asians, especially in breast cancer and prostate cancer. But it was necessary to complete several large samples studies of various type cancers from different ethnic populations. © 2017

Wu Z.,McMaster University | Li S.,Capital Medical University | Lei J.,Tianjin Huan Hu Hospital | An D.,Capital Medical University | And 3 more authors.
American Journal of Neuroradiology | Year: 2010

BACKGROUND AND PURPOSE: SWI is an MR imaging technique that is very sensitive to hemorrhage. Our goal was to compare SWI and CT to determine if SWI can show traumatic SAH in different parts of the subarachnoid space. MATERIALS AND METHODS: Twenty acute TBI patients identified by CT with SAH underwent MR imaging scans. Two neuroradiologists analyzed the CT and SWI data to decide whether there were SAHs in 8 anatomical parts of the subarachnoid space. RESULTS: Fifty-five areas with SAH were identified by both CT and SWI. Ten areas were identified by CT only and 13 by SWI only. SAH was recognized on SWI by its very dark signal intensity surrounded by CSF signal intensity in the sulci or cisterns. Compared with the smooth-looking veins, SAH tended to have a rough boundary and inhomogeneous signal intensity. In many instances, blood in the sulcus left an area of signal intensity loss that had a "triangle" shape. SWI showed 5 more cases of intraventricular hemorrhage than did CT. CONCLUSIONS: SAH can be recognized by SWI through its signal intensity and unique morphology. SWI can provide complementary information to CT in terms of small amounts of SAH and hemorrhage inside the ventricles.

Zhang C.,University of Houston | Zhang C.,Tianjin Huan Hu Hospital | Moore L.M.,University of Houston | Li X.,University of Houston | And 3 more authors.
Neuro-Oncology | Year: 2013

Isocitrate dehydrogenase (IDH) enzymes have recently become a focal point for research aimed at understanding the biology of glioma. IDH1 and IDH2 are mutated in 50%-80% of astrocytomas, oligodendrogliomas, oligoastrocytomas, and secondary glioblastomas but are seldom mutated in primary glioblastomas. Gliomas with IDH1/2 mutations always harbor other molecular aberrations, such as TP53 mutation or 1p/19q loss. IDH1 and IDH2 mutations may serve as prognostic factors because patients with an IDH-mutated glioma survive significantly longer than those with an IDH-wild-type tumor. However, the molecular pathogenic role of IDH1/2 mutations in the development of gliomas is unclear. The production of 2-hydroxyglutarate and enhanced NADP+ levels in tumor cells with mutant IDH1/2 suggest mechanisms through which these mutations contribute to tumorigenesis. Elucidating the pathogenesis of IDH mutations will improve understanding of the molecular mechanisms of gliomagenesis and may lead to development of a new molecular classification system and novel therapies. © The Author(s) 2013. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved.

Zhu Y.,Tianjin Huan Hu Hospital | Zhu L.,Wenzhou University | Lu L.,Tianjin Medical University | Zhang L.,Tianjin Huan Hu Hospital | And 3 more authors.
Oncology Reports | Year: 2014

Ether lipids have been implicated in the exacerbation of human tumors. Accumulating evidence suggests that the alkylglycerone phosphate synthase (AGPS) is involved in the suppression of some types of tumor. However, the role and molecular mechanism of AGPS in the invasion of human glioma and hepatic carcinoma remain unclear. In the present study, using AGPS-knockdown human glioma U87 and hepatic carcinoma HepG2 cell lines, we explored the role of AGPS, as well as its molecular mechanism, in invasion in vitro. It was demonstrated that silencing AGPS expression resulted in a decreased expression of cellular lipids such as LPA, LPAe and PGE2, adhesion, invasion potential and arrested cell cycle in tumor cells. The expression of invasion-related genes such as MMP-2/9, E-cadherin and CD44 showed marked changes in AGPS-knockdown cells. In addition, we found that AGPS regulated the activity of the MAPK pathway, as well as the transcriptional activity of Twist, AP-1, and Snail. The results demonstrated that AGPS negatively regulated the invasion potential of glioma and hepatic carcinoma cells by modulating the expression of relevant genes and activity of the MAPK pathway. Therefore, AGPS may be a potential glioma and hepatic carcinoma therapeutic target.

Zhang C.,Tianjin Huan Hu Hospital | Peng G.,University of Texas M. D. Anderson Cancer Center
Mutation Research - Reviews in Mutation Research | Year: 2015

Non-coding RNAs play a crucial role in maintaining genomic stability which is essential for cell survival and preventing tumorigenesis. Through an extensive crosstalk between non-coding RNAs and the canonical DNA damage response (DDR) signaling pathway, DDR-induced expression of non-coding RNAs can provide a regulatory mechanism to accurately control the expression of DNA damage responsive genes in a spatio-temporal manner. Mechanistically, DNA damage alters expression of a variety of non-coding RNAs at multiple levels including transcriptional regulation, post-transcriptional regulation, and RNA degradation. In parallel, non-coding RNAs can directly regulate cellular processes involved in DDR by altering expression of their targeting genes, with a particular emphasis on miRNAs and lncRNAs. MiRNAs are required for almost every aspect of cellular responses to DNA damage, including sensing DNA damage, transducing damage signals, repairing damaged DNA, activating cell cycle checkpoints, and inducing apoptosis. As for lncRNAs, they control transcription of DDR relevant gene by four different regulatory models, including signal, decoy, guide, and scaffold. In addition, we also highlight potential clinical applications of non-coding RNAs as biomarkers and therapeutic targets for anti-cancer treatments using DNA-damaging agents including radiation and chemotherapy. Although tremendous advances have been made to elucidate the role of non-coding RANs in genome maintenance, many key questions remain to be answered including mechanistically how non-coding RNA pathway and DNA damage response pathway is coordinated in response to genotoxic stress. © 2014 Elsevier B.V.

Dong C.,Tianjin Huan Hu Hospital
Drug research | Year: 2015

Cadmium (Cd) is a potent neurotoxic heavy metal, known to induce oxidative stress and membrane disturbances in brain. Proanthocyanidins (PACs), the most abundant polyphenol class in the human diet, have protective effects on oxidative stress and other metabolic disorders. Based on the cellular protective effect of PACs, we aimed to investigate whether PACs could protect the neuronal cells from Cd-induced excitotoxicity. The experiment was carried out on mice model and also in primary culture of hippocampal neurons isolated from neonatal mice. The Cd-induced changes in acetylcholinesterase (AChE) activity, oxidative stress markers (lipid peroxidation/lipid hydroperoxidation), antioxidant status and Akt phosphorylation were measured in the mice brain with or without PACs treatment. Mice intoxicated with cadmium (5 mg/kg/day) for 4 weeks had significantly (p<0.05) reduced the AChE levels, elevated the levels of oxidative stress markers along with the significant (p<0.05) decrease in the levels of both enzymatic antioxidants and non-enzymatic antioxidants in mice brain tissue. In contrast, administration of PACs (100 mg/kg/day) for 4 weeks in cadmium-intoxicated mice had significantly (p<0.05) protected the cadmium-mediated changes. In addition, PACs treatment in cultured mice hippocampal neurons had protected Cd-induced excitotoxicity by activating Akt phosphorylation, decreasing the caspase-3 level and improving the neuronal cell survival rate up to 24 h. Altogether, our data suggest that PACs plays a crucial role on neuroprotection in combating the cadmium induced oxidative neurotoxicity in mice brain by influencing the activation of AChE/Akt phosphorylation, antioxidant status, controlling the membrane damage (lipid peroxidation) and apoptotic protein caspase-3. © Georg Thieme Verlag KG Stuttgart · New York.

Chun-zhi Z.,Tianjin Medical University | Chun-zhi Z.,Tianjin Huan Hu Hospital | Lei H.,Tianjin Medical University | An-ling Z.,Tianjin Medical University | And 7 more authors.
BMC Cancer | Year: 2010

Background: MicroRNAs (miRNAs) can function as either oncogenes or tumor suppressor genes via regulation of cell proliferation and/or apoptosis. MiR-221 and miR-222 were discovered to induce cell growth and cell cycle progression via direct targeting of p27 and p57 in various human malignancies. However, the roles of miR-221 and miR-222 have not been reported in human gastric cancer. In this study, we examined the impact of miR-221 and miR-222 on human gastric cancer cells, and identified target genes for miR-221 and miR-222 that might mediate their biology.Methods: The human gastric cancer cell line SGC7901 was transfected with AS-miR-221/222 or transduced with pMSCV-miR-221/222 to knockdown or restore expression of miR-221 and miR-222, respectively. The effects of miR-221 and miR-222 were then assessed by cell viability, cell cycle analysis, apoptosis, transwell, and clonogenic assay. Potential target genes were identified by Western blot and luciferase reporter assay.Results: Upregulation of miR-221 and miR-222 induced the malignant phenotype of SGC7901 cells, whereas knockdown of miR-221 and miR-222 reversed this phenotype via induction of PTEN expression. In addition, knockdonwn of miR-221 and miR-222 inhibited cell growth and invasion and increased the radiosensitivity of SGC7901 cells. Notably, the seed sequence of miR-221 and miR-222 matched the 3'UTR of PTEN, and introducing a PTEN cDNA without the 3'UTR into SGC7901 cells abrogated the miR-221 and miR-222-induced malignant phenotype. PTEN-3'UTR luciferase reporter assay confirmed PTEN as a direct target of miR-221 and miR-222.Conclusion: These results demonstrate that miR-221 and miR-222 regulate radiosensitivity, and cell growth and invasion of SGC7901 cells, possibly via direct modulation of PTEN expression. Our study suggests that inhibition of miR-221 and miR-222 might form a novel therapeutic strategy for human gastric cancer. © 2010 Chun-zhi et al; licensee BioMed Central Ltd.

Zhu Y.,Tianjin Huan Hu Hospital | Zhuang J.-X.,Tianjin Baodi Hospital | Wang Q.,Tianjin Huan Hu Hospital | Zhang H.-Y.,Tianjin Baodi Hospital | Yang P.,Tianjin Huan Hu Hospital
Asian Pacific Journal of Cancer Prevention | Year: 2013

Malignant glioma, also known as brain cancer, is the most common intracranial tumor, having an extremely high mortality and recurrence rate. The survival rate of the affected patients is very low and treatment is difficult. Hence, growth inhibition of glioma has become a hot topic in the study of brain cancer treatment. Among the various isothiocyanate compounds, it has been confirmed that benzyl isothiocyanate (BITC) can inhibit the growth of a variety of tumors, including leukemia, glioma and lung cancer, both inside and outside the body. This study explored inhibitory effects of BITC on human glioma U87MG cells, as well as potential mechanisms. It was found that BITC could inhibit proliferation, induce apoptosis and arrest cell cycling of U87MG cells. In addition, it inhibited the expression of SOD and GSH, and caused oxidative stress to tumor cells. Therefore, it is believed that BITC can inhibit the growth of U87MG cells outside the body. Its mechanism may be related to the fact that BITC can cause oxidative stress to tumor cells.

Liu J.,Tianjin Medical University | Liu J.,Tianjin Huan Hu Hospital | Xu X.,Tianjin First Center Hospital | Feng X.,Tianjin First Center Hospital | And 2 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2011

Glioblastoma multiforme (GBM) carries a dismal prognosis primarily due to its aggressive proliferation in the brain regulated by complex molecular mechanisms. One promising molecular target in GBM is over-expressed basic fibroblast growth factor (bFGF), which has been correlated with growth, progression, and vascularity of human malignant gliomas. Previously, we reported significant antitumor effects of an adenovirus-vector carrying bFGF small interfering RNA (Ad-bFGF-siRNA) in glioma in vivo and in vitro. However, its mechanisms are unknown. Signal transducer and activator of transcription 3 (STAT3) is constitutively active in GBM and correlates positively with the glioma grades. In addition, as a specific transcription factor, STAT3 serves as the convergent point of various signaling pathways activated by multiple growth factors and/or cytokines. Therefore, we hypothesized that the proliferation inhibition and apoptosis induction by Ad-bFGF-siRNA may result from the interruption of STAT3 phosphorylation. In the current study, we found that in glioma cells U251, Ad-bFGF-siRNA impedes the activation of ERK1/2 and JAK2, but not Src, decreases IL-6 secretion, reduces STAT3 phosphorylation, decreases the levels of downstream molecules CyclinD1 and Bcl-xl, and ultimately results in the collapse of mitochondrial membrane potentials as well as the induction of mitochondrial-related apoptosis. Our results offer a potential mechanism for using Ad-bFGF-siRNA as a gene therapy for glioma. To our knowledge, it is the first time that the bFGF knockdown using adenovirus-mediated delivery of bFGF siRNA and its potential underlying mechanisms are reported. Therefore, this finding may open new avenues for developing novel treatments against GBM. © 2011 Liu et al; licensee BioMed Central Ltd.

Yan Y.,Tianjin Huan Hu Hospital | Wang Q.,Tianjin Huan Hu Hospital | Yan X.-L.,Tianjin Huan Hu Hospital | Zhang Y.,Tianjin Medical University | And 4 more authors.
FEBS Letters | Year: 2015

MicroRNAs (miRNAs) play a critical role in the development of cancers. However, the role of miRNAs in glioma is still poorly understood. In this study, we demonstrate that microRNA-10a (miR-10a) promotes cell migration and invasion by negatively regulating the expression of Eph tyrosine kinase receptor A8 (EphA8). Ectopic expression of EphA8 counteracts the promotion of migration and invasion induced by miR-10a. We further demonstrate that miR-10a and EphA8 regulate epithelial-mesenchymal transition (EMT) to affect cell migration and invasion. Collectively, we unveil a branch of the miR-10a/EphA8 pathway that regulates the progression of glioma. © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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