70 research outputs found
Addition of Graphite Filler to Enhance Electrical, Morphological, Thermal, and Mechanical Properties in Poly (Ethylene Terephthalate): Experimental Characterization and Material Modeling
Poly(ethylene terephthalate)/graphite (PET/G) micro-composites were fabricated by the melt compounding method using a minilab extruder. The carbon fillers were found to act as nucleating agents for the PET matrix and hence accelerated crystallization and increased the degree of crystallinity. TGA showed that carbon fillers improved the resistance to thermal and thermo-oxidative degradation under both air and nitrogen atmospheres. However, a poor agreement was observed at higher loadings of the filler where the composites displayed reduced reinforcement efficiency. The results demonstrate that the addition of graphite at loading >14.5 wt.% made electrically conductive composites. It was calculated that the electric conductivities of PET/graphite micro-composites were enhanced, above the percolation threshold values by two orders of magnitudes compared to the PET matrix. The minimum value of conductivity required to avoid electrostatic charge application of an insulating polymer was achieved, just above the threshold values. The addition of graphite also improved thermal stability of PET, accelerated its crystallization process and increased the degree of crystallinity. Microscopic results exhibit no indication of aggregations at 2 wt.% graphite, whereas more agglomeration and rolling up could be seen as the graphite content was increased in the PET matrix (in particular, above the percolation threshold value). Furthermore, based on the mechanical experimental characterization of the PET/graphite micro-composites, a large deformation-based mathematical model is proposed for material behavior predictions. The model fits well the experimental data and predicts other mechanical data that are not included in the parameter identification
MicroRNA-211 Expression Promotes Colorectal Cancer Cell Growth In Vitro and In Vivo by Targeting Tumor Suppressor CHD5
Background: Chromodomain-helicase-DNA-binding protein 5 (CHD5) is a newly identified tumor suppressor that is frequently downregulated in a variety of human cancers. Our previous work revealed that the low expression of CHD5 in colorectal cancer is correlated with CHD5 promoter CpG island hypermethylation. In this study, we investigated the effect of microRNA-211 (miR-211)-regulated CHD5 expression on colorectal tumorigenesis. Methodology/Principal Findings: miR-211 was predicted to target CHD5 by TargetScan software analysis. A stably expressing exogenous miR-211 colorectal cancer cell line (HCT-116 miR-211) was generated using lentiviral transduction and used as a model for in vitro and in vivo studies. The expression level of miR-211 in HCT-116 miR-211 cells was upregulated by 16-fold compared to vector control cells (HCT-116 vector). Exogenous miR-211 directly binds to the 39-untranslated region (39-UTR) of CHD5 mRNA, resulting in a 50 % decrease in CHD5 protein level in HCT-116 miR-211 cells. The levels of cell proliferation, tumor growth, and cell migration of HCT-116 miR-211 cells were significantly higher than HCT-116 vector cells under both in vitro and in vivo conditions, as determined using the methods of MTT, colony formation, flow cytometry, scratch assay, and tumor xenografts, respectively. In addition, we found that enforced expression of miR-211 in HCT-116 cells was able to alter p53 pathway-associated regulatory proteins, such as MDM2, Bcl-2, Bcl-xL, and Bax. Conclusion/Significance: Our results demonstrate that CHD5 is a direct target of miR-211 regulation. Enforced expression o
LGR6 Is a High Affinity Receptor of R-Spondins and Potentially Functions as a Tumor Suppressor
BACKGROUND: LGR6 (leucine-rich repeat containing, G protein-coupled receptor 6) is a member of the rhodopsin-like seven transmembrane domain receptor superfamily with the highest homology to LGR4 and LGR5. LGR6 was found as one of the novel genes mutated in colon cancer through total exon sequencing and its promoter region is hypermethylated in 20-50% of colon cancer cases. In the skin, LGR6 marks a population of stem cells that can give rise to all cell lineages. Recently, we and others demonstrated that LGR4 and LGR5 function as receptors of R-spondins to potentiate Wnt/Ī²-catenin signaling. However, the binding affinity and functional response of LGR6 to R-spondins, and the activity of colon cancer mutants of LGR6 have not been determined. PRINCIPAL FINDINGS: We found that LGR6 also binds and responds to R-spondins 1-3 with high affinity to enhance Wnt/Ī²-catenin signaling through increased LRP6 phosphorylation. Similar to LGR4 and LGR5, LGR6 is not coupled to heterotrimeric G proteins or to Ī²-arrestin following R-spondin stimulation. Functional and expression analysis of three somatic mutations identified in colon cancer samples indicates that one mutant fails to bind and respond to R-spondin (loss-of-function), but the other two have no significant effect on receptor function. Overexpression of wild-type LGR6 in HeLa cells leads to increased cell migration following co-treatment with R-spondin1 and Wnt3a when compared to vector control cells or cells overexpressing the loss-of-function mutant. CONCLUSIONS: LGR6 is a high affinity receptor for R-spondins 1-3 and potentially functions as a tumor suppressor despite its positive effect on Wnt/Ī²-catenin signaling
Dietary methyl donors, methyl metabolizing enzymes, and epigenetic regulators: dietāgene interactions and promoter CpG island hypermethylation in colorectal cancer
Dietary methyl donors might influence DNA methylation during carcinogenesis of colorectal cancer (CRC). Among 609 CRC cases and 1,663 subcohort members of the Netherlands Cohort Study on diet and cancer (nĀ =Ā 120,852), we estimated CRC risk according to methyl donor intake across genotypes of folate metabolizing enzymes and methyltransferases
Effect of Exposure to 900 MHz GSM Mobile Phone Radiofrequency Radiation on Estrogen Receptor Methylation Status in Colon Cells of Male Sprague Dawley Rats
Background: Over the past several years, the rapidly increasing use of mobile
phones has raised global concerns about the biological effects of exposure to radiofrequency
(RF) radiation. Numerous studies have shown that exposure to electromagnetic
fields (EMFs) can be associated with effects on the nervous, endocrine, immune,
cardiovascular, hematopoietic and ocular systems. In spite of genetic diversity, the
onset and progression of cancer can be controlled by epigenetic mechanisms such as
gene promoter methylation. There are extensive studies on the epigenetic changes of
the tumor suppressor genes as well as the identification of methylation biomarkers in
colorectal cancer. Some studies have revealed that genetic changes can be induced by
exposure to RF radiation. However, whether or not RF radiation is capable of inducing
epigenetic alteration has not been clarified yet. To date, no study has been conducted
on the effect of radiation on epigenetic alterations in colorectal cancer (CRC). Several
studies have also shown that methylation of estrogen receptor Ī± (ERĪ±), MYOD,
MGMT, SFRP2 and P16 play an important role in CRC. It can be hypothesized that
RF exposure can be a reason for the high incidence of CRC in Iran. This study aimed
to investigate whether epigenetic pattern of ERĪ± is susceptible to RF radiation and if
RF radiation can induce radioadaptive response as epigenetic changes after receiving
the challenge dose (Ī³-ray).
Material and Method: 40 male Sprague-Dawley rats were divided into 4 equal
groups (Group I: exposure to RF radiation of a GSM cell phone for 4 hours and sacrificed
after 24 hours; Group II: RF exposure for 4 hours, exposure to Co-60 gamma
radiation (3 Gy) after 24 hours and sacrificed after 72 hrs; Group III: only 3Gy gamma
radiation; Group 4: control group). DNA from colon tissues was extracted to evaluate
the methylation status by methylation specific PCR.
Results: Our finding showed that exposure to GSM cell phone RF radiation was capable
of altering the pattern of ERĪ± gene methylation compared to that of non-exposed
controls. Furthermore, no adaptive response phenomenon was induced in the pattern
of ERĪ± gene methylation after exposure to the challenging dose of Co-60 Ī³-rays.
Conclusion: It can be concluded that exposure to RF radiation emitted by GSM
mobile phones can lead to epigenetic detrimental changes in ERĪ± promoter methylation
pattern
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