Shenyang, China
Shenyang, China

Shenyang Medical College is a medical institution of higher learning in Shenyang, Liaoning Province, P. R. China. It was formerly known as Shenyang Municipal Advanced Practice Nurse School . The school opened in 1949 and was renamed Shenyang Advanced Medical School, directly managed under the provincial administration, in 1958. It was upgraded to Shenyang Medical College in 1987. The college expanded in size, increased the number of specialties offered and improved in operations. It established a multi-tier education system involving bachelor degree education, advanced diploma education and adult education. It graduated more than 20,000 students. Wikipedia.

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Zhou W.,Shenyang Medical College | Wang G.,Xavier University of Louisiana | Guo S.,Morehouse School of Medicine
Biochimica et Biophysica Acta - Reviews on Cancer | Year: 2013

Breast cancer angiogenesis is elicited and regulated by a number of factors including the Notch signaling. Notch receptors and ligands are expressed in breast cancer cells as well as in the stromal compartment and have been implicated in carcinogenesis. Signals exchanged between neighboring cells through the Notch pathway can amplify and consolidate molecular differences, which eventually dictate cell fates. Notch signaling and its crosstalk with many signaling pathways play an important role in breast cancer cell growth, migration, invasion, metastasis and angiogenesis, as well as cancer stem cell (CSC) self-renewal. Therefore, significant attention has been paid in recent years toward the development of clinically useful antagonists of Notch signaling. Better understanding of the structure, function and regulation of Notch intracellular signaling pathways, as well as its complex crosstalk with other oncogenic signals in breast cancer cells will be essential to ensure rational design and application of new combinatory therapeutic strategies. Novel opportunities have emerged from the discovery of Notch crosstalk with inflammatory and angiogenic cytokines and their links to CSCs. Combinatory treatments with drugs designed to prevent Notch oncogenic signal crosstalk may be advantageous over λ secretase inhibitors (GSIs) alone. In this review, we focus on the more recent advancements in our knowledge of aberrant Notch signaling contributing to breast cancer angiogenesis, as well as its crosstalk with other factors contributing to angiogenesis and CSCs. © 2013 Elsevier B.V.

Bu X.,China Medical University at Heping | Zhao C.,Shenyang Medical College
Tumor Biology | Year: 2013

Cyclooxygenase-2 (COX-2) is proven to influence the carcinogenesis through immune response suppression, apoptosis inhibition, angiogenesis regulation, and tumor cell invasion. Previous studies assessing the association between COX-2 1195 G/A polymorphism and susceptibility to hepatocellular carcinoma (HCC) reported conflicting results. The objective of the study was to investigate the association between COX-2 1195 G/A polymorphism and HCC by a meta-analysis. PubMed, Embase, Web of Science, and Wangfang databases were searched for studies investigating the association between COX-2 1195 G/A polymorphism and HCC risk. The pooled odds ratio (OR) and its 95 % confidence interval (CI) were used to assess the strength of the association. Five studies with a total of 1,690 HCC cases and 1,961 controls were identified. Meta-analyses of total included studies showed that there was an obvious association between COX-2 1195 G/A polymorphism and HCC risk under two main genetic models (for AA versus GG, fixed-effects OR = 1.45, 95 % CI 1.15-1.81, P = 0.001, I 2 = 0.0 %; for AA/GA versus GG, fixed-effects OR = 1.26, 95 % CI 1.05-1.51, P = 0.011, I 2 = 0.0 %). Subgroup analysis by ethnicity showed that association was still obvious in Asians under two genetic models (for AA versus GG, fixed-effects OR = 1.45, 95 % CI 1.16-1.82, P = 0.001, I 2 = 21.7 %; for AA/GA versus GG, fixed-effects OR = 1.27, 95 % CI 1.05-1.54, P = 0.013, I 2 = 0.4 %). The evidence from the meta-analysis supports an association between COX-2 1195 G/A polymorphism and HCC risk in Asians. Further studies with large sample and careful design are needed to identify the possible association in Caucasians. © 2013 International Society of Oncology and BioMarkers (ISOBM).

Liang B.,Shenyang Medical College
European review for medical and pharmacological sciences | Year: 2013

The aim of this study was to investigate serum paraoxonase (PON) activity, arylesterase (ARE) activity, total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) levels in patients with insomnia and to determine whether there was a relationship between oxidative stress and insomnia. A total of 29 insomniacs and 25 healthy controls were recruited in this study. Serum PON and ARE activities, TAS and TOS level were determined, and OSI were calculated. Patients with insomnia had lower PON and ARE activities as compared to healthy controls (PON: 82.0±30.0 U/L vs. 193.5±58.4 U/L, p < 0.001; ARE: 143.0±26.7 U/L vs. 175.0±27.1 U/L, p < 0.001; respectively). Serum TAS was lower, while TOS and OSI were higher in the insomnia group than in the control group (TAS: 1.13±0.29 mmol Trolox equivalent/L vs. 1.70±0.35 mmol Trolox equivalent /L, p < 0.001; TOS: 18.68±5.03 μmol H2O2 equivalent/L vs. 10.92±2.21 μmol H2O2 equivalent/L, p < 0.001; OSI: 1.76±0.74 vs. 0.68±0.23, p < 0.001; respectively). Patients with insomnia have increased systemic oxidative stress and reduced levels of serum antioxidant enzymes. Oxidative stress appears to be an underlying condition associated with insomnia.

Wang Y.,Liaoning Medical University | Zhao W.,Shenyang Medical College | Fu Q.,Liaoning Medical University
Molecular and Cellular Biochemistry | Year: 2013

Accumulating evidence has shown that microRNAs are involved in multiple processes in cancer development and progression. Recently, miR-335 has been identified as a tumor-suppressing microRNA in many human cancers. However, the specific function of miR-335 in osteosarcoma is unclear at this point. In this study, we found that the expression of miR-335 in osteosarcoma tissues and cell lines was much lower than that in normal control, respectively, and the downregulated miR-335 was significantly associated with lymph-node metastasis. Transfection of miR-335 mimics could significantly inhibit the cell migration and invasion in MG-63 and U2OS osteosarcoma cell lines. Moreover, we also showed that ROCK1 was negatively regulated by miR-335 at the posttranscriptional level, via a specific target site within the 3'UTR by luciferase reporter assay. The expression of ROCK1 was inversely correlated with miR-335 expression in osteosarcoma tissues, and knockdown of ROCK1 by siRNA-inhibited osteosarcoma cells migration and invasion resembling that of miR-335 overexpression. Thus, our findings suggest that miR-335 acts as tumor suppressor by targeting the ROCK1 gene and inhibiting osteosarcoma cells migration and invasion. The findings of this study contribute to current understanding of the functions of miR-335 in osteosarcoma. © 2013 Springer Science+Business Media New York.

Ma M.,Shenyang Medical College
Wei sheng yan jiu = Journal of hygiene research | Year: 2011

To investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal development and reproductive endocrine function in prepubertal female rats and its possible mechanisms. 40 female SD rats at 3-week-old were randomly divided into a control group (corn oil) and three exposure groups, which were exposed consecutively for 28 days to DEHP by oral gavage at doses of 50, 150 and 500 mg/(kg x d). The onset of puberty was determined by daily examination for vaginal opening (OV), breast development and the first estrous cycle. By the end of the experiment, the rats were sacrificed during the diestrous stage. The gene expression interrelated with ovary function was detected by real-time PCR. Serum levels of follicle stimulating hormone (FSH) luteinizing hormone (LH), estradiol (E2), progesterone (P4) and testosterone (T) were measured by ELISA. The morphological change of ovaries was observed by HE staining under optical microscope. The expression of PPARgamma protein in ovary cells was measured by immuohistochemistry. The age of vaginal opening was advanced by DEHP exposure in 500 mg/kg group, and the body weight was increased at the time of vaginal opening in 150 and 500 mg/kg groups (P < 0.05). Compared to the control group, the level of T in all DEHP groups was decreased; the levels of FSH and E2 were decreased and the level of P4 was increased in 150 and 500 mg/kg groups (P < 0.05). The gene expression of P4S0Aromin 150 and 500 mg/kg groups was significantly decreased compared to the control group. A significant increase of atretic follicles and a significant reduction of corpora lutea were observed in 150 and 500 mg/kg groups compared to the control group. The expression of PPARgamma protein in granulosa cells of follicle and corpora lutea in 150 and 500 mg/kg groups was higher than that in the control group and 50 mg/kg group (P < 0.05). DEHP exposure can affect the pubertal development and reproductive endocrine function in prepubertal female rats, and its possible mechanism may be correlated with PPARgamma.

Wang P.,Shenyang Medical College
Molecular Therapy | Year: 2016

Aberrant expression of long noncoding RNAs has recently been reported in tumorigenesis and plays a pivotal role in regulating malignant behavior of cancers. In this study, we confirmed that the long noncoding RNAs human histocompatibility leukocyte antigen (HLA) complex P5 (HCP5) was up-regulated in glioma tissues as well as in U87 and U251 cells. Knockdown of HCP5 inhibited the malignant biological behavior of glioma cells by reducing proliferation, migration and invasion, and inducing apoptosis. HCP5 regulated the malignant behavior of glioma cells by binding to microRNA-139, which functions as a tumor suppressor. Moreover, knockdown of HCP5 down-regulated Runt-related transcription factor 1, a direct and functional downstream target of microRNA-139 that is involved in microRNA-139-mediated tumor-suppressive effects in glioma cells. Runt-related transcription factor 1 increased promoter activities and upregulated expression of the oncogenic gene astrocyte elevated gene-1 (AEG-1). Runt-related transcription factor 1 also increased the promoter activities and expression of HCP5, which showed a positive feedback loop in regulating the malignant behavior of glioma cells. In conclusion, this study demonstrated that the HCP5-microRNA-139- Runt-related transcription factor 1 feedback loop plays a pivotal role in regulating the malignant behavior of glioma cells, which may provide a potential therapeutic strategy for treating glioma.Molecular Therapy (2016); doi:10.1038/mt.2016.103. © 2016 American Society of Gene & Cell Therapy

We aimed to investigate the clinical significance of the expression of novel scaffold protein CARMA3 in non-small-cell lung cancer (NSCLC) and the biological function of CARMA3 in NSCLC cell lines. We observed moderate to high CARMA3 staining in 68.8% of 141 NSCLC specimens compared to corresponding normal tissues. The overexpression of CARMA3 was significantly correlated with TNM stage (P = 0.022) and tumor status (P = 0.013). CARMA3 upregulation also correlated with a shorter survival rate of patients of nodal status N0 (P = 0.042)as well as the expression of epidermal growth factor receptor (EGFR) (P = 0.009). In EGFR mutation positive cases, CARMA3 expression was much higher (87.5%) compared to non-mutation cases (66.1%). In addition, we observed that knockdown of CARMA3 inhibits tumor cell proliferation and invasion, and induces cell cycle arrest at the boundary between the G1 and S phase. We further demonstrated a direct link between CARMA3 and NF-κB activation. The change of biological behavior in CARMA3 knockdown cells may be NF-κB-related. Our findings demonstrated, for the first time, that CARMA3 was overexpressed in NSCLC and correlated with lung cancer progression, EGFR expression, and EGFR mutation. CARMA3 could serve as a potential companion drug target, along with NF-kB and EGFR in EGFR-mutant lung cancers.

Hertz L.,Shenyang Medical College
Methods in Molecular Biology | Year: 2012

Protocols are described for measurement in primary cultures of astrocytes of unidirectional fluxes of glutamate (influx and efflux), glutamate metabolism to glutamine or CO 2, glucose influx, glycolysis, pyruvate dehydrogenation, oxidative metabolism of glucose, pyruvate carboxylation, glycogen synthesis, and glycogenolysis. References are made to the in vivo situation, and the importance of using metabolically competent cultures is emphasized. © 2012 Springer Science+Business Media, LLC.

Ma J.,Shenyang Medical College
Journal of Cerebral Blood Flow and Metabolism | Year: 2014

Blood-tumor barrier (BTB) constitutes an efficient organization of tight junctions that impairs the delivery of therapeutic drugs. However, the methods and molecular mechanisms underlying the BTB opening remain elusive. MicroRNAs (miRNAs) have recently emerged as key regulators of various biologic processes and therapeutic targets. In this study, we have identified microRNA-181a (miR-181a) as a critical miRNA in opening BTB. MicroRNA-181a expression was upregulated in glioma endothelial cells (GECs), which were obtained by coculturing endothelial cells (ECs) with glioma cells. Overexpression of miR-181a resulted in an impaired and permeability increased BTB, and meanwhile reduced the expression of zonula occluden (ZO)-1, occludin, and claudin-5. Kruppel-like factor 6 (KLF6), a transcription factor of the zinc-finger family, was downregulated in GECs. Mechanistic investigations defined it as a direct and functional downstream target of miR-181a, which was involved in the regulation of BTB permeability and the expression of ZO-1, occludin, and claudin-5. Furthermore, luciferase assays and chromatin immunoprecipitation assays showed that KLF6 upregulated the promoter activities and interacted with the promoters of ZO-1, occludin, and claudin-5 in GECs. Collectively, we showed the possibility that overexpression of miR-181a contributes to the increased permeability of BTB by targeting KLF6, thereby revealing potential therapeutic targets for the treatment of brain gliomas.Journal of Cerebral Blood Flow and Metabolism advance online publication, 3 September 2014; doi:10.1038/jcbfm.2014.152.

Hertz L.,Shenyang Medical College
Journal of Cerebral Blood Flow and Metabolism | Year: 2011

Inspired by the paper, Brain glutamine synthesis requires neuronal-κBorn aspartate as amino donor for glial glutamate formation by Pardo et al, a modified model of oxidation-reduction, transamination, and mitochondrial carrier reactions involved in aspartate-dependent astrocytic glutamine synthesis and oxidation is proposed. The alternative model retains the need for cytosolic aspartate for transamination of α-ketoglutarate, but the missing aspartate molecule is generated within astrocytes during subsequent glutamate oxidation. Oxaloacetate formed during glutamate formation is used during glutamate degradation, and all transmitochondrial reactions, oxidations-reductions, and cytosolic and mitochondrial transaminations are stoichiometrically balanced. The model is consistent with experimental observations made by Pardo et al. © 2011 ISCBFM All rights reserved.

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