Knockdown of core binding factorβ alters sphingolipid metabolism.

Core binding factor (CBF) is a heterodimeric transcription factor containing one of three DNA-binding proteins of the Runt-related transcription factor family (RUNX1-3) and the non-DNA-binding protein, CBFβ. RUNX1 and CBFβ are the most common targets of chromosomal rearrangements in leukemia. CBF has been implicated in other cancer types; for example RUNX1 and RUNX2 are implicated in cancers of epithelial origin, including prostate, breast, and ovarian cancers.

Down regulation of CSL activity inhibits cell proliferation in prostate and breast cancer cells.

The Notch receptor pathway provides a paradigm for juxtacrine signaling pathways and controls stem cell function, developmental cell fate decisions, and cellular differentiation. The Notch pathway is constitutively activated in human cancers by chromosomal rearrangements, activating point mutations, or altered expression patterns. Therefore, the Notch pathway is the subject of chemotherapeutic intervention in a variety of human cancers.

Association of core-binding factor β with the malignant phenotype of prostate and ovarian cancer cells.

Core binding factor (CBF) is a transcription factor complex that plays roles in development, stem-cell homeostasis, and human disease. CBF is a heterodimer composed of one of three DNA-binding RUNX proteins plus the non-DNA-binding protein, CBFβ. Recent studies have showed that the RUNX factors exhibit complex expression patterns in prostate, breast, and ovarian cancers, and CBF has been implicated in the control of cancer-related genes.

Distinctive degradation behaviors of electrospun polyglycolide, poly(DL-lactide-co-glycolide), and poly(L-lactide-co-epsilon-caprolactone) nanofibers cultured with/without porcine smooth muscle cells.

Biodegradable nanofibers have become a popular candidate for tissue engineering scaffolds because of their biomimetic structure that physically resembles the extracellular matrix. For certain tissue regeneration applications, prolonged in vitro culture time for cellular reorganization and tissue remodeling may be required. Therefore, extensive understanding of cellular effects on scaffold degradation is needed.

Enhancement of neurite outgrowth using nano-structured scaffolds coupled with laminin.

Cell interactions with scaffolds are important for cell and tissue development in the process of repairing and regeneration of damaged tissue. Scaffolds that mimic extracellular matrix (ECM) surface topography, mechanical stiffness, and chemical composition will be advantageous to promote enhanced cell interactions. Electrospinning can easily produce nano-structured synthetic polymer mats with architecture that structurally resembles the ECM of tissue.

Degradation of electrospun nanofiber scaffold by short wave length ultraviolet radiation treatment and its potential applications in tissue engineering.

Development in the field of tissue engineering has brought much attention in the fabrication and preparation of scaffold with biodegradable synthetic polymer nanofibers. Electrospun biodegradable polymeric nanofibers are increasingly being used to fabricate scaffolds for tissue engineering applications as they provide high surface area-to-volume ratio and possess high porosity. One common way to sterilize polymeric nanofiber scaffolds is 254-nm ultraviolet (UV) irradiation.

Long-term viability of coronary artery smooth muscle cells on poly(L-lactide-co-epsilon-caprolactone) nanofibrous scaffold indicates its potential for blood vessel tissue engineering.

Biodegradable polymer nanofibres have been extensively studied as cell culture scaffolds in tissue engineering. However, long-term in vitro studies of cell-nanofibre interactions were rarely reported and successful organ regeneration using tissue engineering techniques may take months (e.g.

Biodegradable polymer nanofiber mesh to maintain functions of endothelial cells.

Maintaining functions of endothelial cells in vitro is a prerequisite for effective endothelialization of biomaterials as an approach to prevent intimal hyperplasia of small-diameter vascular grafts. The aim of this study was to design suitable nanofiber meshes (NFMs) that further maintain the phenotype and functions of human coronary artery endothelial cells (HCAECs). Collagen-coated random and aligned poly(L-lactic acid)-co-poly(epsilon-caprolactone) (P(LLA-CL)) NFMs were fabricated using electrospinning.

Fabrication and endothelialization of collagen-blended biodegradable polymer nanofibers: potential vascular graft for blood vessel tissue engineering.

Electrospun collagen-blended poly(L-lactic acid)-co-poly(epsilon-caprolactone) [P(LLA-CL), 70:30] nanofiber may have great potential application in tissue engineering because it mimicks the extracellular matrix (ECM) both morphologically and chemically. Blended nanofibers with various weight ratios of polymer to collagen were fabricated by electrospinning. The appearance of the blended nanofibers was investigated by scanning electron microscopy and transmission electron microscopy.

Grafting of gelatin on electrospun poly(caprolactone) nanofibers to improve endothelial cell spreading and proliferation and to control cell Orientation.

We modified the surface of electrospun poly(caprolactone) (PCL) nanofibers to improve their compatibility with endothelial cells (ECs) and to show the potential application of PCL nanofibers as a blood vessel tissue-engineering scaffold. Nonwoven PCL nanofibers (PCL NF) and aligned PCL nanofibers (APCL NF) were fabricated by electrospinning technology. To graft gelatin on the nanofiber surface, PCL nanofibers were first treated with air plasma to introduce -COOH groups on the surface, followed by covalent grafting of gelatin molecules, using water-soluble carbodiimide as the coupling agent.

Fabrication of collagen-coated biodegradable polymer nanofiber mesh and its potential for endothelial cells growth.

Endothelialization of biomaterials is a promising way to prevent intimal hyperplasia of small-diameter vascular grafts. The aim of this study was to design a nanofiber mesh (NFM) that facilitates viability, attachment and phenotypic maintenance of human coronary artery endothelial cells (HCAECs). Collagen-coated poly(L-lactic acid)-co-poly(epsilon-caprolactone) P(LLA-CL 70:30) NFM with a porosity of 64-67% and a fiber diameter of 470+/-130 nm was fabricated using electrospinning followed by plasma treatment and collagen coating.

Surface engineering of electrospun polyethylene terephthalate (PET) nanofibers towards development of a new material for blood vessel engineering.

Non-woven polyethylene terephthalate nanofiber mats (PET NFM) were prepared by electrospinning technology and were surface modified to mimic the fibrous proteins in native extracellular matrix towards constructing a biocompatible surface for endothelial cells (ECs). The electrospun PET NFM was first treated in formaldehyde to yield hydroxyl groups on the surface, followed by the grafting polymerization of methacrylic acid (MAA) initiated by Ce(IV). Finally, the PMAA-grafted PET NFM was grafted with gelatin using water-soluble carbodiimide as coupling agent.

Non-viral tumor necrosis factor-alpha gene transfer decreases the incidence of orthotopic bladder tumors.

Our aim was to evaluate the feasibility and efficacy of tumor necrosis factor-alpha gene therapy in preventing bladder tumor recurrence using an orthotopic model of bladder cancer. We transiently transfected a murine bladder cancer cell line MB49 with pBud-TNF-alpha using a transfection system consisting of the cationic liposome N-(1-(2,3-dioleoyloxyl)propyl)-N,N,N-trimethylammoniummethyl sulfate (DOTAP) plus methyl-beta-cyclodextrin solubilized cholesterol (MBC). MB49 cells produced 893.

SKP2 associates with p130 and accelerates p130 ubiquitylation and degradation in human cells.

p130 is a member of the retinoblastoma family of pocket proteins, which includes pRB and p107. Unlike pRB and p107, p130 protein levels decrease dramatically following its hyperphosphorylation starting in the mid-G1 phase of the cell cycle. However, the mechanism leading to p130 downregulation is unknown.

G1 cyclin/cyclin-dependent kinase-coordinated phosphorylation of endogenous pocket proteins differentially regulates their interactions with E2F4 and E2F1 and gene expression.

Mitogenic stimulation leads to activation of G(1) cyclin-dependent kinases (CDKs), which phosphorylate pocket proteins and trigger progression through the G(0)/G(1) and G(1)/S transitions of the cell cycle. However, the individual role of G(1) cyclin-CDK complexes in the coordinated regulation of pocket proteins and their interaction with E2F family members is not fully understood. Here we report that individually or in concert cyclin D1-CDK and cyclin E-CDK complexes induce distinct and coordinated phosphorylation of endogenous pocket proteins, which also has distinct consequences in the regulation of pocket protein interactions with E2F4 and the expression of p107 and E2F1, both E2F-regulated genes.