Publications by authors named "Dan-Feng Sun"

The inkjet printing technology based on piezoelectric micro-jets can effectively realize the efficient and high-precision processing of special-shaped structures. In this work, a nozzle-driven piezoelectric micro-jet device is proposed, and its structure and micro-jet process are described. ANSYS two-phase, two-way fluid-structure coupling simulation analysis is carried out, and the mechanism of the piezoelectric micro-jet is described in detail.

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The enrichment of Enterotoxigenic (ETBF) has been identified in CRC patients and associated with worse prognosis. Cancer stem cells (CSCs) play essential roles in CRC development. However, whether ETBF is involved in CSCs regulation is unknown.

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Reversible post-translational modifications represent a mechanism to control tumor metabolism. Here we show that mitochondrial Sirtuin5 (SIRT5), which mediates lysine desuccinylation, deglutarylation, and demalonylation, plays a role in colorectal cancer (CRC) glutamine metabolic rewiring. Metabolic profiling identifies that deletion of SIRT5 causes a marked decrease in C-glutamine incorporation into tricarboxylic-acid (TCA) cycle intermediates and glutamine-derived non-essential amino acids.

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Colorectal cancer includes an invasive stem-like/mesenchymal subtype, but its genetic drivers, functional, and clinical relevance are uncharacterized. Here we report the definition of an altered miRNA signature defining this subtype that includes a major genomic loss of miR-508. Mechanistic investigations showed that this miRNA affected the expression of cadherin CDH1 and the transcription factors ZEB1, SALL4, and BMI1.

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Zinc finger protein 278 is a zinc finger transcription factor encoded on the 22q12.2 chromosome. Previous studies revealed that ZNF278 expression was significantly upregulated in colorectal cancer (CRC) tissue compared to adjacent non-tumor tissue.

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Objective: To identify genes with aberrant promoter methylation for developing novel diagnostic markers and therapeutic targets against primary colorectal cancer (CRC).

Methods: Two paired CRC and adjacent normal tissues were collected from two CRC patients. A Resi: MBD2b protein-sepharose-4B column was used to enrich the methylated DNA fragments.

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Deregulation of the mammalian target of rapamycin pathway (mTOR pathway) is associated with human cancer. The relationship between mTOR pathway and histone acetylation is still unclear in gastric cancer (GC). Immunohistochemistry was used to examine the phosphorylation of mTOR and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) in GC tissues.

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The polycomb group protein enhancer of zeste homologue 2 (EZH2), which has histone methyltransferase (HMT) activity, is overexpressed in malignant tumours. However, the role of EZH2 in colorectal cancer (CRC) invasion is little known. Here we investigated the clinical significance, biological effects, and mechanisms of EZH2 signalling.

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Production of high quality interpolation maps of heavy metals is important for risk assessment of environmental pollution. In this paper, the spatial correlation characteristics information obtained from Moran's I analysis was used to supplement the traditional geostatistics. According to Moran's I analysis, four characteristics distances were obtained and used as the active lag distance to calculate the semivariance.

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The trafficking protein particle complex 4 (TRAPPC4) is implicated in vesicle-mediated transport, but its association with disease has rarely been reported. We explored its potential interaction with ERK2, part of the ERK1/2 complex in the Extracellular Signal-regulated Kinase/ Mitogen-activated Protein Kinase (ERK-MAPK) pathway, by a yeast two-hybrid screen and confirmed by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down. Further investigation found that when TRAPPC4 was depleted, activated ERK1/2 specifically decreased in the nucleus, which was accompanied with cell growth suppression and apoptosis in colorectal cancer (CRC) cells.

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This study explored the spatial pattern of heavy metals in Beijing agricultural soils using Moran's I statistic of spatial autocorrelation. The global Moran's I result showed that the spatial dependence of Cr, Ni, Zn, and Hg changed with different spatial weight matrixes, and they had significant and positive global spatial correlations based on distance weight. The spatial dependence of the four metals was scale-dependent on distance, but these scale effects existed within a threshold distance of 13 km, 32 km, 50 km, and 29 km, respectively for Cr, Ni, Zn, and Hg.

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Single factor water quality identification index was adopted to assess the surface water quality of Miyun reservoir watershed in Beijing using nearly 20 years monitoring data of 4 sites, also the surface water quality pollution sources were analyzed. The results indicated TP had the largest temporal variation at every monitoring site, coefficients of variation were 93.86%, 86.

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The research object of the present paper is the water quality of Han Shiqiao wetland water. Water spectrum and quality parameters were measured on the site and in the lab. The authors simulated the relationships between water quality parameters and the best bands or combination, and built the multiple linear regression equation to obtain characteristic spectrum of the key water quality parameters.

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The present paper selected Qing yundian town and Weishanzhuang town in Da Xing District, and Gaoling ying town in Shunyi District as test areas, using MODIS data and ASTER data in different scales. The feasibility of winter wheat LAI inversion by PROSAIL physical model, especially the stability of remote sensing data in different scales, was discussed, and the results from experience model inversion were compared with that from statistical methods. The values of all samples LAI inversion from experience model are close in a region, which means experience model is a reflection of general growing trend, ignoring spatial heterogeneity of the regional leaf area index.

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Background: mTOR signaling has been suggested to be an important factor involved in tumorigenesis, but its role in human colorectal cancer (CRC) has not been completely elucidated. Herein, the purpose of this study was to analyze the distribution pattern of mTOR signaling components in CRC and adenoma and to determine whether targeted inhibition of mTOR could be a potential therapeutic strategy for CRC.

Methods: Immunohistochemical analysis was performed on human CRC and adenoma for mTOR signaling components, including mTOR, p70s6 K, and 4EBP1.

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Background And Aims: Although the anticancer effects of rapamycin (RPM) and 5-aza-deoxycytidine (AZA) have been studied extensively, the combined effect of these two drugs on colorectal cancer (CRC) is still unknown. This study addresses the effect of AZA and RPM combination therapy on CRC and its influence on the mammalian target of rapamycin (mTOR) and its signal transduction pathway.

Subjects And Methods: Human CRC cell line HCT116 was treated with AZA alone, RPM alone, or concurrently with a combination of both drugs.

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The role of the mTOR signal pathway in colorectal cancer (CRC) pathogenesis remains unclear, and the combination effect of PD98059 (an inhibitor for MEK) and rapamycin (an inhibitor for mTOR) on CRC is still unknown. Here, we found that combination treatment with PD98059 and rapamycin suppressed the proliferation of CRC cells, induced apoptosis, arrested cell cycle, and reduced the incidence and volume of CRC in mice, as well as inhibited phosphorylation of mTOR and the MEK signal pathway components, of which the effects were more significant than single-drug treatments. These findings indicate that PD98059 combined with rapamycin appears to be a promising strategy for inhibiting the initiation, and progression of CRC, which may provide a novel strategy for CRC prevention.

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Colorectal cancer is a leading cause of morbidity and mortality worldwide, and its incidence has been increasing in recent years. The role of epigenetic modifications, including DNA methylation and histone modifications, has only recently been investigated. In this study, the effects of epigenetic agents such as folic acid (FA) and sodium butyrate (NaBu) on the development of colorectal cancer induced by 1,2-dimethylhydrazine (DMH) using ICR mice was examined.

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The extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK-MAPK) is critical in human malignancies. It remained to be established whether DNA methyltransferases (Dnmt) and proliferating cell nuclear antigen (PCNA) involved in DNA methylation during RAF-transformed cell proliferation. The plasmid of constitutively active RAF was used to transfect gastric cell GES-1 and cancer cell AGS.

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The present study aimed to investigate the effect of knocking-down methylenetetrahydrofolate reductase (MTHFR) on the survival of the human gastric cancer cell line MKN45. Antisense and small interfering RNA (siRNA) plasmids were used to target MTHFR in MKN45. Meanwhile, we also constructed a wild-type MTHFR plasmid to assess the effect of over-expression of this protein on cell viability.

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Objective: To investigate the synergistic effect of rapamycin (RPM) and PD98059 on human colorectal cancer cells and its potential mechanisms.

Methods: Three human colorectal cancer cell lines SW480, HCT116 and HT29 were treated with RPM 10 nmol/L, PD98059 (10 micromol/L, 20 micromol/L, 40 micromol/L, 50 micromol/L), or RPM plus PD98059, respectively, and the sensitivity was analyzed by MTT assay. The cell cycle progression was evaluated by flow cytometry.

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DNA methylation is an epigenetic modification associated with gene transcription regulation, X-chromosome inactivation, regulation of development and cell differentiation. Aberrant DNA methylation has been linked to cancer. The advent of microarray technology has provided new opportunities for high-throughput study on DNA methylation.

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Abnormalities in the STAT3 pathway are involved in the oncogenesis of several cancers. However, the mechanism by which dysregulated STAT3 signaling contributes to the progression of human colorectal cancer (CRC) has not been elucidated, nor has the role of JAK, the physiological activator of STAT3, been evaluated. To investigate the role of both JAK and STAT3 in CRC progression, we inhibited JAK with AG490 and depleted STAT3 with a SiRNA.

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