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Pancreatic cancer is a fatal disease across the world with 5 years survival rate less than 10%. ATAD2, a valid cancer drug-target, is overexpressed in pancreatic malignancy with high oncogenic potential. However, the mechanism of the upregulated expression of ATAD2 in pancreatic cancer is unknown. Since microRNAs (miRNAs) could potentially control target mRNA expressions, and are involved in cancer as tumor-suppressors, oncomiR or both, we examine the possibility of miRNA-mediated regulation of ATAD2 in pancreatic cancer cells (PCCs). Our in-silico approach first identifies hsa-miR-217 as a candidate regulator for ATAD2 expression. For further validation, luciferase reporter assay is performed. We overexpress hsa-miRNA-217 and assess cellular viability, migration, apoptosis and cell cycle progression in three different PCCs (BxPC3, PANC1, and MiaPaCa2). We find hsa-miRNA-217 has potential binding site at the 3′UTR of ATAD2. Luciferase assay confirms that ATAD2 is a direct target of hsa-miR-217. Overexpression of hsa-miR-217 drastically downregulates ATAD2 expression in PCCs, thus, corroborating binding studies. The elevated expression of hsa-miRNA-217 diminishes cell proliferation and migration as well as induces apoptosis and cell cycle arrest in PCCs. Finally, siRNA mediated ATAD2 knockdown or overexpression of hsa-miRNA-217 in PCCs showed inactivation of the AKT signaling pathway. Therefore, hsa-miR-217 abrogates pancreatic cancer progression through inactivation of the AKT signaling pathway and this might be partly due to miR-217 mediated suppression of ATAD2 expression. The application of hsa-miR-217 mimic could be a promising therapeutic strategy for the treatment of pancreatic cancer patients in near future. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract: A commercial epoxy diglycidylether of bisphenol-A (DGEBA) was modified by adding fluorinated poly(aryl ether ketone) fluoropolymer and in turn metal micro powders (Ni, Al, Zn, and Ag) and coated on mild steel. Two curing agents were used; triethylenetetramine (a low temperature curing agent) and hexamethylenediamine (a high temperature curing agent) for understanding the curing temperature effect on the properties. Variations in tribological properties (dynamic friction and wear) and surface energies with varying amounts of metal powders and curing agents were evaluated. When cured at 30°C, dynamic friction and wear decrease significantly due to phase separation reaction being favored between the fluoropolymer and the epoxy. However, when cured at 80°C, friction and wear increase; this can be explained in terms of a crosslinking reaction favored at that temperature. There is a significant decrease in surface energies with the addition of modifiers. [Copyright &y& Elsevier]

ATAD2 is a promising oncoprotein with tumor-promoting functions in many cancers. It is a valid cancer drug-target and a potential cancer-biomarker for multiple malignancies. As a cancer/testis antigen (CTA), ATAD2 could also be a probable candidate for immunotherapy. It is a unique CTA that belongs to both AAA+ ATPase and bromodomain family proteins. Since 2007, several research groups have been reported on the pleiotropic oncogenic functions of ATAD2 in diverse signaling pathways, including Rb/E2F-cMyc pathway, steroid hormone signaling pathway, p53 and p38-MAPK-mediated apoptotic pathway, AKT pathway, hedgehog signaling pathway, HIF1α signaling pathway, and Epithelial to Mesenchymal Transition (EMT) pathway in various cancers. In all these pathways, ATAD2 participates in chromatin dynamics, DNA replication, and gene transcription, demonstrating its role as an epigenetic reader and transcription factor or coactivator to promote tumorigenesis. However, despite the progress, an overall mechanism of ATAD2-mediated oncogenesis in diverse origin is elusive. In this review, we summarize the accumulated evidence to envision the overall ATAD2 signaling networks during carcinogenesis and highlight the area where missing links await further research. Besides, the structure-function aspect of ATAD2 is also discussed. Since the efforts have already been initiated to explore targeted drug molecules and RNA-based therapeutic alternatives against ATAD2, their potency and prospects have been elucidated. Together, we believe this is a well-rounded review on ATAD2, facilitating a new drift in ATAD2 research, essential for its clinical implication as a biomarker and/or cancer drug-target. [Display omitted] • ATAD2 is a promising oncoprotein, a valid cancer target and a potential biomarker. • ATAD2 is an AAA+ ATPase, a cancer/testis antigen and a bromodomain family protein. • Upregulated ATAD2 activates many signaling pathways in cancer. • MicroRNAs identified to target ATAD2, function as tumor suppressor. • Drug discovery initiatives show bromodomain of ATAD2 is a druggable target. [ABSTRACT FROM AUTHOR]

We report the optimisation of the experimental variables for the synthesis of large-area (90 cm 2 ), mm-thick carpets of vertically aligned multi-wall carbon nanotubes (MWCNTs) using the aerosol-assisted chemical vapour deposition technique. The effect of the reactor size, temperature, time and the flow rate of the carrier gas on the catalytic conversion rate of the precursor, composition of the atmosphere of the reactor and various properties of MWCNTs such as the mass, length, outer diameter, defect density, oxidation resistance and residual catalyst concentration was investigated. By increasing the volume of the reactor from around 0.2 to 8.5 L, the mass of synthesised MWCNTs and the efficiency of the precursor were increased fivefold (up to 14 g/h.) and twice (up to 88%), respectively. Free-standing and on-substrate carpets of MWCNTs could withstand normal handling without falling apart, making them suitable for characterisations and applications from nano to macro scales. The synthesis recipe also improved the production rate of nitrogen-containing MWCNTs by an order of magnitude. [ABSTRACT FROM AUTHOR]