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"Zhi, Xiaofei"
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تاريخ التبادلات الأدبية الصينية العربية
ترصد موسوعة \"تاريخ التبادلات الأدبية الصينية العربية\" مسيرة التبادلات الثقافية والأدبية منذ القدم بين الحضارتين الصينية والعربية، والترجمات الصينية الأولى للأدب العربي، كما تسلط الضوء على الأدب الصيني في الدول العربية، ورحلة التبادلات بين الأدباء العرب والصينيين والأحداث التاريخية التي واكبت محطات حركة التبادلات الأدبية بين الجانبين. كما ترصد التاريخ الطويل للأمة العربية في التواصل التجاري والثقافي والأدبي مع الصين، حيث عرفت الصين العرب منذ القرن الثاني قبل الميلاد مع رحلة المبعوث الصيني تشانغ تشيان إلى الغرب في عصر الإمبراطور هان وو دي، ثم عبر طريق الحرير البري القديم وطريق الحرير البحري \"طريق التوابل\" اللذين شهدا تدفقا للتجار العرب على الصين لتنتعش التبادلات الثقافية والأدبية إلى جانب التجارية بين الجانبين يوما بعد يوم.
Book
Ubiquitin‐specific peptidase 24 accelerates aerobic glycolysis and tumor progression in gastric carcinoma through stabilizing PLK1 to activate NOTCH1
Ubiquitin‐specific peptidase 24 (USP24), a member of the deubiquitinase family, plays an important role in tumor regulation. However, the role of USP24 in gastric cancer (GC) is unknown. The aim of our study was to explore the role of USP24 in GC to seek new therapeutic targets for GC. TCGA analysis showed that USP24 was upregulated in GC patients, and its high expression levels were associated with poor prognosis. It was found that overexpressed USP24 promoted GC cell proliferation and abnormal glycolysis. Further analysis and study showed that USP24 could promote the stability and increase the expression of oncogene PLK1. Knocking down USP24 can reduce the stability of PLK1 to reduce Notch 1 activity, thus inhibiting GC glycolysis, proliferation, and other processes and alleviating tumor progression. Knocking down USP24 can inhibit GC progression. In conclusion, USP24 was upregulated in GC and promoted the growth and glycolysis of GC cells, the mechanism of which was related to the deubiquitination of PLK1 and the increase of its stability. Silencing USP24 inhibited the GC process. This study suggests that the USP24/PLK1/Notch 1 axis may be a novel therapeutic target for gastric cancer. Our study found that USP24 is highly expressed in GC, which is an indicator of the prognosis of GC patients. This is because USP24 promotes glycolysis of GC cells by upregulating PLK1 and activating the Notch signaling pathway, thus promoting the progress of GC, which may provide a basis for the treatment of GC and a new treatment option.
Journal Article
Adrenergic modulation of AMPK-dependent autophagy by chronic stress enhances cell proliferation and survival in gastric cancer
Epidemiological data show that chronic stress has adverse effects on the incidence and progression of cancer. As a critical target organ for stress hormones, the stomach is frequently subjected to stress-related injury. However, few reports regarding the association between stress and gastric cancer (GC) have been published. The present study aimed to investigate the effect of chronic stress on the growth and survival of GC, and the role of the autophagy process. A restraint-stress procedure over 21 days was used to establish a chronic stress mouse model. Subcutaneous xenografts and gastric orthotopic xenografts were established in BALB/c nude mice. Alzet osmotic minipumps containing either PBS or propranolol hydrochloride was inserted on the nape of the neck 7 days prior to the initiation of restraint stress. The presence of autophagosomes and autolysosomes were examined by electron microscopy. The stress hormone norepinephrine significantly enhanced the proliferation of GC cells. By inhibiting adrenoreceptor expression, it was demonstrated that β2-adrenergic receptor (ADRB2) was the specific β-adrenergic receptor subtype responsible for catecholamine release. In addition, it was demonstrated that the induction of autophagy was a novel consequence of β2-adrenergic activation in GC cells. This was demonstrated by the appearance of double-membrane vesicles, punctuate GFP-RFP-microtubule-associated protein 1 light chain 3 distribution in the cytoplasm and a corresponding increase in autophagic flux. Notably, norepinephrine-induced autophagy was shown to have a tumor-promoting role under conditions of chronic stress in vitro and in vivo. It was further demonstrated that, upon activation of cAMP-response element binding protein, chronic stress promoted autophagic flux through the adenosine 5′-monophosphate-activated protein kinase-unc-51 like autophagy activating kinase 1 (AMPK-ULK1) pathway. Tissue microarray analysis revealed a negative correlation between the expression of ADRB2 and autophagic marker p62/sequestosome-1 in GC tumor samples. Additionally, high protein levels of ADRB2 correlated positively with tumor, node, metastasis stage and poor prognosis in patients with GC. These results establish a novel pathway that chronic stress activates tumor-promoting autophagy to accelerate the progression of GC. The present study is the first, to the best of our knowledge, providing preclinical evidence that chronic stress serves a role in the progression of GC.
Journal Article
miR-874 Inhibits cell proliferation, migration and invasion through targeting aquaporin-3 in gastric cancer
Background
Aquaporin-3 (AQP3) is a water transporting protein which plays an oncogenic role in several malignant tumors. However, its regulatory mechanism remains elusive to date. In this study, we investigated the microRNA-mediated gene repression mechanism involved in AQP3's role.
Methods
The potential microRNAs targeting
AQP3
were searched via bioinformatic methods and identified by luciferase reporter assays, microRNA RT–PCR and western blotting. The expression patterns of miR-874 and AQP3 in human gastric cancer (GC) specimens and cell lines were determined by microRNA RT-PCR and western blotting. 5-ethynyl-2′-deoxyuridine, cell migration and invasion assays and tumorigenicity in vivo were adopted to observe the effects of miR-874 depletion or ectopic miR-874 expression on GC cell phenotypes. Cell apoptosis was evaluated by FACS and TUNEL in vitro and in vivo respectively.
Results
miR-874 suppressed AQP3 expression by binding to the 3′UTR of
AQP3
mRNA in GC cells. miR-874 was significantly down-regulated and reversely correlated with AQP3 protein levels in clinical samples. Analysis of the clinicopathological significance showed that miR-874 and AQP3 were closely correlated with GC characteristics. Functional analyses indicated that ectopic miR-874 expression suppressed the growth, migration, invasion and tumorigenicity of GC cells, whereas miR-874 knockdown promoted these phenotypes. Down-regulation of Bcl-2, MT1-MMP, MMP-2 and MMP-9 and upregulation of caspase-3 activity and Bax were involved in miR-874 inducing cell apoptosis, and inhibiting migration and invasion.
Conclusions
These results provide a mechanism by which AQP3 is upregulated, as well as highlight the importance of miR-874 in gastric cancer development and progression.
Journal Article
Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway
Background
Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear.
Methods
RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.
Results
In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling.
Conclusion
We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future.
Journal Article
Laparoscopic versus Open Total Gastrectomy for Gastric Cancer: An Updated Meta-Analysis
To expand the current knowledge on the feasibility and safety of laparoscopic total gastrectomy (LTG) for gastric cancer in comparison with open total gastrectomy (OTG).
Additional studies comparing laparoscopic versus open total gastric resection have been published, and it is necessary to update the meta-analysis of this subject.
Original articles compared LTG and OTG for gastric cancer, which published in English from January 1990 to July 2013 were searched in PubMed, Embase, and Web of Knowledge by two reviewers independently. Operative time, blood loss, harvested lymph nodes, proximal resection margin, analgesic medication, first flatus day, first oral intake, postoperative hospital stay, postoperative complications, hospital mortality, 5-year overall survival (OS) and disease-free survival (DFS) were compared using STATA version 10.1.
17 studies were selected in this analysis, which included a total of 2313 patients (955 in LTG and 1358 in OTG). LTG showed longer operative time, less blood loss, fewer analgesic uses, earlier passage of flatus, quicker resumption of oral intake, earlier hospital discharge, and reduced postoperative morbidity. The number of harvested lymph nodes, proximal resection margin, hospital mortality, 5-year OS and DFS were similar.
LTG had the benefits of less blood loss, less postoperative pain, quicker bowel function recovery, shorter hospital stay and lower postoperative morbidity, at the price of longer operative time. There were no statistical differences in lymph node dissection, resection margin, hospital mortality, and long-term outcomes, which indicated the similar oncological safety with OTG. A positive trend was indicated towards LTG. So LTG can be performed as an alternative to OTG by the experienced surgeons in high-volume centers. Whereas, due to the relative small sample size of long-term outcomes and lack of randomized control trials, more studies are required.
Journal Article
miR-27b-3p suppresses cell proliferation through targeting receptor tyrosine kinase like orphan receptor 1 in gastric cancer
Background
The receptor tyrosine kinase-like orphan receptors (ROR) family contains the atypical member ROR1, which plays an oncogenic role in several malignant tumors. However, the clinical potentials and underlying mechanisms of ROR1 in gastric cancer progression remain largely unknown. In this study, we validated the microRNA-mediated gene repression mechanism involved in the role of ROR1.
Methods
Bioinformatic prediction, luciferase reporter assay, quantitative real-time PCR (qRT-PCR) and western blotting were used to reveal the regulatory relationship between miR-27b-3p and ROR1. The expression patterns of miR-27b-3p and ROR1 in human gastric cancer (GC) specimens and cell lines were determined by microRNA RT-PCR and western blotting. Cell proliferation, colony formation assay in soft agar
in vitro
and tumorigenicity
in vivo
were performed to observe the effects of downregulation and upregulation miR-27b-3p expression on GC cell phenotypes.
Results
miR-27b-3p suppressed ROR1 expression by binding to the 3’UTR of ROR1 mRNA in GC cells. miR-27b-3p was significantly downregulated and reversely correlated with ROR1 protein levels in clinical samples. Analysis of the clinicopathological significance showed that miR-27b-3p and ROR1 were closely correlated with GC characteristics. Ectopic miR-27b-3p expression suppressed cell proliferation, colony formation in soft agar, xenograft tumors of GC cells. By contrast, miR-27b-3p knockdown enhanced these malignant behaviors. Our studies further revealed that the c-Src/STAT3 signaling pathway was involved in miR-27b-3p-ROR1-mediated cell proliferation regulation.
Conclusions
These results show that miR-27b-3p suppresses ROR1 expression through the binding site in the 3’UTR inhibiting the cell proliferation. These findings indicate that miR-27b-3p exerts tumor-suppressive effects in GC through the suppression of oncogene ROR1 expression and suggest a therapeutic application of miR-27b-3p in GC.
Journal Article
Practical Role of Mutation Analysis for Imatinib Treatment in Patients With Advanced Gastrointestinal Stromal Tumors: A Meta-Analysis
Imatinib has become the standard first line treatment of gastrointestinal stromal tumors (GIST) in the advanced phase and adjuvant setting. We carried out an up-to-date meta-analysis to determine the practical role of mutation analysis for imatinib treatment in patients with advanced GIST.
Eligible studies were limited to imatinib treatment for patients with advanced GIST and reported on mutation analysis. Statistical analyses were conducted to calculate the odds ratio (OR), hazard ratio (HR) and 95% confidence interval (CI) using fixed-effects and random-effects models.
A total of 2834 patients from 3 randomized controlled trials and 12 cohort studies were included. The ORs of response rates in KIT exon 11-mutant GISTs were 3.504 (95% CI 2.549-4.816, p<0.001) and 3.521 (95% CI 1.731-7.165, p=0.001) compared with KIT exon 9-mutant and wild type GISTs, respectively. The HRs of progression-free survival in KIT exon 11-mutant GISTs were 0.365 (95% CI 0.301-0.444, p<0.001) and 0.375 (95% CI 0.270-0.519, p<0.001) compared with KIT exon 9-mutant and wild type GISTs. The HRs of overall survival in KIT exon 11-mutant GISTs were 0.388 (95% CI 0.293-0.515, p<0.001) and 0.400 (95% CI 0.297-0.538, p<0.001) compared with KIT exon 9-mutant and wild type GISTs. No statistical significant differences were found between KIT exon 9-mutant and wild type. The overall response rate in KIT-exon 11-mutant GISTs were 70.5% (65%-75.9%) compared with 57.1% (51%-63.2%) in KIT-positive GISTs. No evidence of publication bias was observed.
Patients with advanced GIST harboring a KIT exon 11 mutation have the best response rate and long-term survival with imatinib treatment. Mutation analysis would be more helpful than KIT expression analysis to decide appropriate therapy for a specific patient.
Journal Article
Prognostic role of microscopically positive margins for primary gastrointestinal stromal tumors: a systematic review and meta-analysis
The impact and management of microscopically positive margins in gastrointestinal stromal tumors (GISTs) remain unclear. The aim of this study is to estimate the prognostic value of surgical margins for disease-free survival (DFS) and overall survival (OS) in patients with primary GISTs. Twelve studies with 1985 GIST patients were included. The overall recurrence rate in R1 resection and R0 resection group was 0.364 (95% CI 0.299–0.429) and 0.296 (95% CI 0.161–0.430), respectively. Meta-analysis confirmed that a microscopically positive margin could significantly impact the disease-free survival (HR 1.596, 95% CI 1.128–2.258; I
2
= 37.5%, P value = 0.091), but had no influence on overall survival (HR 1.430, 95% CI 0.608–3.363; I
2
= 60.8%, P value = 0.013). Importantly, subgroup analysis revealed that adjuvant imatinib treatment could attenuate the risk of recurrence for primary GIST patients who received R1 resection. (HR 1.308, 95% CI 0.583–2.935; I
2
= 53.2%, P value = 0.074). The level of evidence achieved in this study was “moderate” for DFS and “low” for OS. In conclusion, this study revealed that a microscopically positive margin is an unfavorable prognostic factor for GIST patients with R1 resection and adjuvant imatinib treatment is proved to be effective.
Journal Article
CEP55 contributes to human gastric carcinoma by regulating cell proliferation
Centrosomal protein 55 (CEP55) is the latest found member in the centrosomal relative protein family, which participates in cell-cycle regulation. CEP55 exists in many kinds of normal tissues and tumour cells such as hepatocellular carcinoma, and is important in carcinogenesis. However, the role of CEP55 in the pathogenesis of gastric cancer (GC) remains unclear. The mRNA levels of CEP55 in GC tissues and GC cell lines were examined by quantitative real-time PCR, and the protein expression of CEP55 in GC tissues was detected by Western blot and immunohistochemistry. The role of CEP55 in regulating the proliferation of GC cell lines was investigated both in vitro and in vivo. CEP55 was strongly upregulated in human GC, indicating that CEP55 contributed to carcinogenesis and progression of GC. Ectopic overexpression of CEP55 enhanced the cell proliferation, colony formation, and tumourigenicity of GC cells, whereas CEP55 knockdown inhibited these effects. We discovered that cell transformation induced by CEP55 was mediated by the AKT signalling pathway. Overexpression of CEP55 enhanced the phosphorylation of AKT and inhibited the activity of p21 WAF1/Cip1. In addition, cellular proliferation was suppressed as a result of cell cycle arrest at the G2/M phase in CEP55-knockdown cells. CEP55 expression was elevated in GC compared with normal control tissues. Credible evidence showed that CEP55 can be a potential therapeutic target in GC.
Journal Article