bluuebunny/crossref_metadata_2025_split huggingface dataset:
miR‐145 is a potential biomarker for predicting clinical outcome in glioblastomas
Authors: Shi Lei , Wang Bin , Gu Xiaoyan , Zhang Shuguang , Li Xiaoliang , Zhu Haifeng 
Published: November 2018

AbstractmiR‐145 has been found to be significantly downregulated in gliomas, and overexpression of miR‐145 increases glioma cell apoptosis and enhances chemosensitivity or herpes simplex virus thymidine kinase gene therapy. However, the correlation between miR‐145 and the clinical prognosis of glioblastomas has never been explored. In this study, a retrospective study was conducted in 86 cases of patients with glioblastoma after neurosurgery combined with chemoradiotherapy, and 36 cases with traumatic brain injury. Our results showed that miR‐145 was significantly lower in glioblastoma tissues than that in normal brain tissue (P < 0.05). Furthermore, miR‐145 was lower in patients with lower Karnofsky Performance Scale (KPS) scores than in patients with higher KPS scores (
P < 0.05). Cox Regression analysis showed that low miR‐145 expression was associated with poor patient survival (
P < 0.05). These data suggested that patients with glioblastoma with lower miR‐145 expression are prone to shorter overall survival.
Acetyl‐coenzyme A acyltransferase 2 promote the differentiation of sheep precursor adipocytes into adipocytes
Authors: Zhang Yani , Wang Yingjie , Wang Xiaoyan , Ji Yanqin , Cheng Shaoze , Wang Man , Zhang Chen , Yu Xinjian , Zhao Ruifeng , Zhang Wenhui , Jin Jing , Li Tingting , Zuo Qisheng , Li Bichun 
Published: November 2018

AbstractThe acetyl CoA acyltransferase 2 (ACAA2) is a key enzyme of the fatty acid oxidation pathway, catalyzing the last step of the mitochondrial beta oxidation, thus playing an important role in the fatty acid metabolism. The purpose of this study was to investigate the effect of knocking out ACAA2 on the expression of genes lipoprteinlipase (LPL), peroxisome proliferator‐activated receptor‐γ (PPAR‐γ), fatty acid synthase, fat mass and obesity‐associated gene, adipocyte fatty acid‐binding protein (AP2) in precursor adipocytes and their differentiation into adipocytes. The knockout vector was constructed using CRISPR‐Cas RNA‐guided nuclease technology with an efficiency of 23.80%, and the vector was transfected into precursor adipocyte cells, while an overexpression vector of the ACAA2 gene was also transfected in another group of preadipocytes. Quantitative polymerase chain reaction showed that the expression of the PPAR‐γ, LPL, and AP2 was significantly lower in the knockout compared with the overexpression group, while there was no difference in cell growth. After induction of adipocyte precursor cells into adipocytes using dexamethasone, insulin, and IBMX, oil red staining showed a significantly different number of lipid droplets in the knockout group. These results provide a preliminary indication for a possible involvement of the ACAA2 gene in adipocyte differentiation in vitro.
Retracted: Combined therapy using LHRH‐PE40 and anti‐CD40 dendritic cells substantially eliminate tumor cells
Authors: Zhang Limin , Du TianJiao , Ma DongBin , Guo Fang , Li ZhenWei , Yan Hua 
Published: November 2018

AbstractLHRH‐PE40 was used to promote the proliferation of bone marrow derived cell (BMDC) and improve the antigen‐presenting ability of BMDC as well as the immune function via the CD40 signal pathway. LHRH‐PE40 was also implicated in cancer treatment, targeting a variety of cancer cells that express luteinizing hormone‐releasing hormone receptor (LHRHR). In the present study, the mechanism and efficacy of LHRH‐PE40 were addressed in the following three aspects. Enzyme‐linked immunosorbent assay was performed to confirm the binding specificity of LHRH‐PE40 to LHRHR. The killing effect of LHRH‐PE40 on target cells was mediated by LHRHR, which specifically killed LHRHR‐positive target cells while the minimal cytotoxicity of LHRHR‐negative cells is negligible. Spiegelmers, a molecule mutually exclusive with GnRH and developed by Sven Klussmann and Dr Sven Klussmann of NOXXON Pharmaceuticals in Germany, demonstrated that LHRH‐PE40 maintains a combinatory characteristics of LHRH and LHRHR. In the end, the mechanism of LHRH‐PE40 underlying induction of apoptosis at low concentration and prolonged conditions was firstly demonstrated by the basic method of detecting apoptosis to induce apoptosis. It provided a scientific basis for clinical application of LHRH‐PE40 and laid a foundation for the further study of LHRH‐PE40 on inducing apoptosis of target cells. The target cells herein refer to tumor cells that overexpress LHRHR. This study shows that activated DC can more effectively promote the proliferation of CD4+ T cells, and initially proved that DC carrying anti‐CD40 antibody promoted the immune treatment of the tumor. Combining LHRH‐PE40 with anti‐CD40 DCs achieved substantially improved efficacy in killing tumor cells.
Long noncoding RNA LINC00968 promotes endothelial cell proliferation and migration via regulating miR‐9‐3p expression
Authors: Wang Xiaofeng , Zhao Zheng , Zhang Wei , Wang Yi 
Published: November 2018

AbstractLong noncoding RNAs (lncRNAs) have been showed to play a crucial role in pathogenesis and development of cardiovascular diseases. Our study aimed to study the expression and functional role of lncRNA LINC00968 in the development of coronary artery disease (CAD). We showed that the LINC00968 expression level was upregulated in the CAD tissues compared with normal arterial tissues. In addition, we showed that the expression level of LINC00968 was upregulated by oxidized low‐density lipoprotein (oxLDL) treatment in endothelial cell. Ectopic expression of LINC00968 regulated the proliferation and migration of endothelial cell. Moreover, we showed that overexpression of LINC00968 inhibited miR‐9‐3p expression in an endothelial cell. Furthermore, we demonstrated that the miR‐9‐3p expression was downregulated in the CAD samples compared with normal arterial tissues and the expression level of miR‐9‐3p was downregulated by oxLDL treatment in endothelial cell. Finally, we showed that ectopic expression of LINC00968 promoted endothelial cell proliferation and migration partly through regulating miR‐9‐3p expression. These results suggested that LINC00968 plays a crucial role in the progression of the CAD.
Long noncoding RNA HOXD‐AS2 regulates cell cycle to promote glioma progression
Authors: Qi Yingjiao , Wang Zhixing , Wu Fan , Yin Bin , Jiang Tao , Qiang Boqin , Yuan Jiangang , Han Wei , Peng Xiaozhong 
Published: November 2018

AbstractNow, numerous exciting findings have been found that long noncoding RNAs (lncRNAs) play a vital role in cancer malignant progression. However, their potential involvement in glioma is not well understood. Here, we performed a high‐throughput microarray to detect the lncRNA expression profiles between glioma cell lines and normal astrocyte cell lines. HOXD‐AS2 was increased in glioma cells and it was associated with glioma grade and poor prognosis. Loss of HOXD‐AS2 can inhibit glioma cell growth by inducing cell‐cycle G1 arrest in vitro. The proliferation of glioma was inhibited followed by knocking down the expression of HOXD‐AS2 not only in subcutaneous injection model but also in orthotopic implantation model. These findings indicate that HOXD‐AS2 promotes the glioma progression and may serve as a potential target for glioma diagnosis and therapy.
Retracted: microRNA‐145 regulates tumor suppressor candidate 3 and mitogen‐activated protein kinase pathway to inhibit the progression of colorectal cancer
Authors: Tang Hanqing , Li Keming , Zheng Jianyu , Dou Xibin , Zhao Yufeng , Wang Luyao 
Published: November 2018

AbstractBackgroundIt has been reported that microRNA‐145 (miR‐145) is downregulated in various cancers, including colorectal cancer (CRC). However, the role of miR‐145 in progress of CRC and its mechanism remains unclear.MethodsThe expressions of miR‐145 and tumor suppressor candidate 3 (TUSC3) were determined in CRC tissues and cells by real‐time quantitative polymerase chain reaction and Western blot analysis. The effects of miR‐145 and TUSC3 on cell viability, migration, and invasion of CRC cells were examined by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐trtrazolium bromide assay and trans‐well chamber experiment, respectively. The interaction between miR‐145 and TUSC3 was explored by bioinformatics analysis, luciferase reporter assay, and Western blot analysis. The abundances of mitogen‐activated protein kinase (MAPK) signaling pathway‐related proteins were measured by Western blot analysis.ResultsmiR‐145 expression was downregulated in CRC tissues and cell lines, and TUSC3 was upregulated in CRC tissues and correlated inversely with miR‐145 abundance. Overexpression of miR‐145 and knockdown of TUSC3 suppressed cell viability, migration, and invasion in LS174T and HCT116 cells. Moreover, TUSC3 was indicated as a novel target of miR‐145 and its expression was negatively regulated by miR‐145. Restoration of TUSC3 can partially reverse the inhibitory effects of miR‐145 on phosphorylation of extracellular signal‐regulated kinases 1 and 2 in CRC cells.ConclusionmiR‐145 can inhibit the viability, migration, and invasion through addressing MAPK signaling pathway by targeting TUSC3 in CRC cells, providing a novel biomarker for treatment of CRC.
A novel role and mechanism of cystic fibrosis transmembrane conductance regulator in bisphenol A‐induced prostate cancer
Authors: Zhu Xiaonian , Gao Li , Yan Chengmei , He Yonghua 
Published: November 2018

AbstractBisphenol A (BPA) is a well known environmental endocrine disruptor that may cause human prostate cancer through disturbing cell mitosis, proliferation, and apoptosis. As one of the most important anion channels in organisms, cystic fibrosis transmembrane conductance regulator (CFTR) is proposed as a tumor suppressor in carcinogenesis and development of prostate cancer in recent studies. Whether CFTR plays a role in BPA‐induced prostate cancer needs to be further identified. In this study, two prostate cancer cell lines PC‐3 and LNCaP were exposed to BPA for detecting the cytotoxic reactions by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide and enzyme‐linked immunosorbent assays. After the treatment with BPA for 24 hours, the cell viability was decreased significantly with increased cell apoptosis in the two cell lines. Moreover, both PC‐3 and LNCaP cells had a reduced expression level of cAMP, CFTR, and adenosine triphosphate upon BPA treatment. In addition, AMPKα kinase was found upregulated to promote cell apoptosis through increasing Bax expression and decreasing Bcl‐2 expression. Our study suggests a role and mechanism of CFTR in BPA‐induced prostate cancer via cell apoptosis for the first time.
Sulfated hyaluronic acid and dexamethasone possess a synergistic potential in the differentiation of osteoblasts from human bone marrow stromal cells
Authors: Schmidt Johannes R. , Vogel Sarah , Moeller Stephanie , Kalkhof Stefan , Schubert Kristin , von Bergen Martin , Hempel Ute 
Published: November 2018

AbstractThe development of novel bioactive biomaterials is urgently needed to meet the needs of an aging population. Both sulfated hyaluronic acid and dexamethasone are candidates for the functionalization of bone grafts, as they have been shown to enhance the differentiation of osteoblasts from bone marrow stromal cells in vitro and in vivo. However, the underlying mechanisms are not fully understood. Furthermore, studies combining different approaches to assess synergistic potentials are rare. In this study, we aim to gain insights into the mode of action of both sulfated hyaluronic acid and dexamethasone by a comprehensive analysis of the cellular fraction, released matrix vesicles, and the extracellular matrix, combining classical biochemical assays with mass spectrometry–based proteomics, supported by novel bioinformatical computations. We found elevated differentiation levels for both treatments, which were further enhanced by a combination of sulfated hyaluronic acid and dexamethasone. Single treatments revealed specific effects on osteogenic differentiation. Dexamethasone activates signalling pathways involved in the differentiation of osteoblasts, for example, CXC‐motif chemokine receptor type 4 and mitogen‐activated protein kinases. The effects of sulfated hyaluronic acid were predominantly linked to an alteration in the composition of the extracellular matrix, affecting the synthesis, secretion, and/or activity of fibrillary (fibronectin and thrombospondin‐2) and nonfibrillary (transglutaminase‐2, periostin, and lysyloxidase) extracellular matrix components, including proteases and their inhibitors (matrix metalloproteinase‐2, tissue inhibitor of metalloproteinase‐3). The effects were treatment specific, and less additive or contrary effects were found. Thus, we anticipate that the synergistic action of the treatment‐specific effects is the key driver in elevated osteogenesis.
BMP2/7 heterodimer enhances osteogenic differentiation of rat BMSCs via ERK signaling compared with respective homodimers
Authors: Miao Chunlei , Qin Dengke , Cao Peigang , Lu Ping , Xia Yutong , Li Mengjiao , Sun Miao , Zhang Wei , Yang Fanghong , Zhang Yingjie , Tang Shengjian , Liu Tianyi , Liu Fangjun 
Published: November 2018

AbstractBone morphogenetic protein (BMP)2/7 heterodimer shows greater efficacy in enhancing bone regeneration. However, the precise mechanism and the role of mitogen‐activated protein kinase (MAPK) signaling network in BMP2/7‐driven osteogenesis remain ambiguous. In this study, we evaluated the effects of BMP2/7 heterodimers on osteoblastic differentiation in rat bone marrow mesenchymal stem cells (BMSCs), with the aim to elaborate how MAPKs might be involved in this cellular process by treatment of rat BMSCs with BMP2/‐7 with a special signal‐pathway inhibitor. We found that BMP2/7 heterodimer induced a much stronger osteogenic response in rat BMSCs compared with either homodimer. Most interestingly, extracellular signal‐regulated kinase (ERK) demonstrated a highly sustained phosphorylation and activation in the BMP2/7 heterodimer treatment groups, and inhibition of ERK cascades using U0126 special inhibitor that significantly reduced the activity of ALP and calcium mineralization to a substantial degree in rat BMSCs treated with BMP2/7 heterodimers. Collectively, we demonstrate that BMP2/7 heterodimer shows a potent ability to stimulate osteogenesis in rat BMSCs. The activated ERK signaling pathway involved in this process may contribute partially to an increased osteogenic potency of heterodimeric BMP2/7 growth factors.
Parathyroidectomy decreases serum intact parathyroid hormone and calcium levels and prolongs overall survival in elderly hemodialysis patients with severe secondary hyperparathyroidism
Authors: Wan Jinnan , Li Wenhuan , Zhong Yuan 
Published: November 2018

BackgroundThe objective of this study was to assess the effect of parathyroidectomy (PTX) treatment on prolonging overall survival (OS) as well as decreasing levels of intact parathyroid hormone (iPTH), calcium (Ca), and phosphorus (P) in elderly hemodialysis patients with severe secondary hyperparathyroidism (SHPT).MethodsA total of 304 elderly hemodialysis patients with severe SHPT were consecutively enrolled in this cohort study. According to whether PTX operations were applied, patients were classified into PTX group (N = 112) and Control group (N = 192) and were followed up for 3 years. Mortality rate and OS were evaluated, and iPTH, Ca, and P levels were recorded.ResultsCompared to control group, increased iPTH (P < 0.001), higher Ca (P = 0.003), elevated AST (P = 0.022), and lower Hb (P = 0.049) concentrations were observed in the PTX group at baseline. The 1‐year mortality (P < 0.001), 2‐year mortality (P < 0.001), and 3‐year mortality (P < 0.001) was reduced in PTX group compared to Control group, and PTX was correlated with prolonged OS (P < 0.001). Multivariate Cox's regression analysis further revealed that PTX treatment (P < 0.001, HR = 0.177) was an independent factor for better OS. Moreover, patients in PTX group had decreased iPTH (P < 0.05) and Ca (P < 0.05) levels compared to Control group at M1‐M36, while no difference was found in serum P level between the two groups at M1‐M36.ConclusionParathyroidectomy decreases iPTH and Ca levels, and it associates with favorable survival in elderly hemodialysis patients with severe SHPT.
Efficacy of different hemodialysis methods on dendritic cell marker CD40 and CD80 and platelet activation marker CD62P and P10 in patients with chronic renal failure
Authors: Wang Xin‐Fang , Zhang Bei‐Hao , Lu Xiao‐Qing , Wang Pei 
Published: November 2018

BackgroundChronic renal failure (CRF) has become a major public health concern, which increases the risk of stroke and systemic thromboembolism. Therefore, therapeutic strategies are in urgent requirement. This study was conducted for investigating efficacy of hemodialysis (HD), hemodiafiltration (HDF), and hemoperfusion (HP) in patients with CRF and the correlation with the presence of complications following HD therapy.MethodsThe therapeutic effect, living quality, biochemical indicators, and dry weight were detected before and after the treatment regimens. Flow cytometry was conducted to detect expressions of dendritic cell markers (CD40 and CD80) and platelet activation markers (CD62P and P10), and the relationship between their expression and therapeutic effect as well as the association of these expressions with complications was analyzed.ResultsAfter HD therapy, patients presented with decreased serum creatinine, serum phosphorus, triglyceride, parathyroid hormone, and β2‐MG expression; increased hemoglobin, plasma albumin expressions, and dry weight; and enhanced therapeutic effect and living quality. CD62P and P10 expressions decreased, while CD40 and CD80 expressions increased following HD therapy. The therapeutic effect improved in patients with low expressions of CD40 and CD80 and high expressions of CD62P and P10 following HP treatment and complications were lower after treatment of HDF and HP.ConclusionThe aforementioned results indicated that CRF patients treated with HP exhibited higher expression of CD40 and CD80 and lower expression of CD62P and P10, suggesting that HP is conferred to have better efficacy than HDF and HD. Therefore, HP may be a promising clinical regimen for treatment of CRF patients.
Fusobacterium nucleatum and colorectal cancer: A mechanistic overview
Authors: Hashemi Goradel Nasser , Heidarzadeh Siamak , Jahangiri Samira , Farhood Bagher , Mortezaee Keywan , Khanlarkhani Neda , Negahdari Babak 
Published: November 2018

AbstractColorectal cancer (CRC) is the third most prevalent cancer in the world. There are many risk factors involved in CRC. According to recent findings, the tumor microenvironment and feces samples of patients with CRC are enriched by Fusobacterium nucleatum. Thus,
F. nucleatum is proposed as one of the risk factors in the initiation and progression of CRC. The most important mechanisms of
Fusobacterium nucleatum involved in CRC carcinogenesis are immune modulation (such as increasing myeloid‐derived suppressor cells and inhibitory receptors of natural killer cells), virulence factors (such as FadA and Fap2), microRNAs (such as miR‐21), and bacteria metabolism. The aim of this review was to evaluate the mechanisms underlying the action of
F. nucleatum in CRC.
The novel relationship between Sirt3 and autophagy in myocardial ischemia–reperfusion
Authors: Zheng Yitian , Shi Binhao , Ma Mengqing , Wu Xiaoqin , Lin Xianhe 
Published: November 2018

AbstractClass III histone deacetylases (HDACs) belong to the proteasome family, comprising seven family members identified in mammalian cells, identified Sirt1–Sirt7. As an important member of HDACs, Sirt3 is hotly debated for its multiple functions. It was reported that Sirt3 got involved in the alleviation of multiple diseases, including myocardial infarction, neuron ischemia, hypertrophy, and diabetic myopathy. Through regulating many cellular mechanisms, such as apoptosis, autophagy, and clearance of reactive oxygen species (ROS), Sirt3 played an important role in the alleviation of myocardial ischemia–reperfusion injury. Nowadays Sirt3‐induced autophagy was indicated to be involved in the process of the development of myocardial ischemia–reperfusion injury. Sirt3 could both activate and inhibit autophagy process by activating different downstream signal pathways, such as Sirt3–AMP‐activated protein kinase pathway, Sirt3–Foxo3a pathway, and Sirt3–superoxide dismutase–mitochondrial ROS pathway. Whereas the Sirt3‐induced autophagy in different phases of myocardial ischemia–reperfusion has not been systematically illustrated. In this review, we summarized the regulated mechanisms found in these years and listed the updated research about the relationship between Sirt3 and autophagy which are both positive and negative during myocardial ischemia–reperfusion phase. We anticipated that we may controlled the activation of autophagy by regulating the concentration of Sirt3 in myocyte. By maintaining a proper expression of autophagy in different phases of myocardial ischemia–reperfusion, we could reduce the morbidity of patients with myocardial infarction apparently in the future.
Identification of the potential prognostic genes of human melanoma
Authors: Wang Bing , Qu Xing‐Long , Chen Yong 
Published: November 2018

AbstractThe melanoma is one of the most dangerous forms of skin diseases. It may spread to other parts of the body and cause serious illness and death. Early detection and diagnosis are crucial. However, the systemic expression analysis for the different staging of melanoma is still lacking to date. In this study, we analyzed the gene expression profiles of the different staging of melanoma by the differential expression analysis and random forest analysis. First, the results of the principal component analysis showed that the clustering of primary tumor samples, normal samples, and pigment nevus samples got closer, while the clustering of tumor metastatic samples and normal samples was far away. Moreover, the gene expression of tumor metastasis stage and the initial stage had obvious differences. Almost 426 genes identified had differential expression. The functional enrichment of differentially expressed genes was associated with the epidermal cell differentiation, epidermis development, and the keratinocyte differentiation. Taken together, our findings identified the differentially expressed signatures between primary melanoma and metastatic melanoma. Our results would provide the potential mechanisms of melanoma.