ACSL4 upregulates IFI44 and IFI44L expression and promotes the proliferation and invasiveness of head and neck squamous cell carcinoma cells.

Reprogramming of cellular energy metabolism, including deregulated lipid metabolism, is a hallmark of head and neck squamous cell carcinoma (HNSCC). However, the underlying molecular mechanisms remain unclear. Long-chain acyl-CoA synthetase 4 (ACSL4), which catalyzes fatty acids to form fatty acyl-CoAs, is critical for synthesizing phospholipids or triglycerides.

ACK1 upregulated the proliferation of head and neck squamous cell carcinoma cells by promoting p27 phosphorylation and degradation.

Head and neck squamous cell carcinoma (HNSCC) is a malignancy with a worldwide distribution. Although intensive studies have been made, the underlying oncogenic mechanism of HNSCC requires further investigation. In this study, we examined the oncogenic role of activated Cdc42-associated kinase 1 (ACK1), an oncogenic tyrosine kinase, in regulating the proliferation of HNSCC cells and its underlying molecular mechanism.

Anti-Proliferative Effect of Statins Is Mediated by DNMT1 Inhibition and p21 Expression in OSCC Cells.

Statins, also known as HMG-CoA reductase inhibitors, are a class of cholesterol-lowering drugs and their anti-cancer effects have been studied in different types of malignant diseases. In the present study, we investigated the anti-proliferative effects of statins, including cerivastatin and simvastatin, on oral squamous cell carcinoma (OSCC) cells. Our data showed that statins inhibited the proliferation of three OSCC cell lines in a dose-dependent manner and this growth inhibition was confirmed through G/G cell cycle arrest.

p66Shc regulates migration of castration-resistant prostate cancer cells.

Metastatic castration-resistant (CR) prostate cancer (PCa) is a lethal disease for which no effective treatment is currently available. p66Shc is an oxidase previously shown to promote androgen-independent cell growth through generation of reactive oxygen species (ROS) and is elevated in clinical PCa and multiple CR PCa cell lines. We hypothesize p66Shc also increases the migratory activity of PCa cells through ROS and investigate the associated mechanism.

Crowned Ionic Liquids for Biomolecular Interaction Analysis.

On the basis of affinity recognition with positively charged side chains in peptides and proteins, a series of crowned 1,2,3-triazolium ionic liquids (CIL 1-6) was developed and found to be capable of quantitatively extracting peptides and proteins from the aqueous layer into the ionic liquid phase. All of the synthesized CIL 1-6 are liquid at room temperature. This is the first example of biomolecular recognition of both lysine- and arginine-containing peptides and proteins by CILs in pure ionic liquid phase.

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells.

Androgen receptor (AR) is a steroid hormone receptor that functions as a transcription factor for regulating cell growth and survival. Aberrant AR function becomes a risk factor for promoting the progression of prostate cancer (PCa). In this study, we examined the roles of proline-rich tyrosine kinase 2 (PYK2) and ribosomal S6 kinase 1 (S6K1) in regulating AR expression and activity and growth properties in PCa cells.

Three-dimensional reconstruction of trachea using computed tomography imaging as therapy for tracheal stenosis in infants.

Background And Objective: In this study, we aim to develop a system that uses computed tomography (CT) imaging for three-dimensional (3D) reconstruction of the trachea as therapy for tracheal stenosis in infants, and further calculate the cross-sectional area and volume, assisting doctors in clinical diagnosis.

Methods: We first used image processing, calculating the cross-sectional area and volume. We used the improved median filter for image processing and designed the system for capturing the cross-sectional area of endotracheal tube.

Tyrosine 397 phosphorylation is critical for FAK-promoted Rac1 activation and invasive properties in oral squamous cell carcinoma cells.

Oral squamous cell carcinoma (OSCC) is a common cancer worldwide. Despite advances in diagnosis and therapy, treatment options for patients with metastatic OSCC are few, due in part to the limited understanding of the molecular events involved in the invasion and metastasis of OSCC. In this study, we investigated the expression of focal adhesion kinase (FAK) and its tyrosine 397 phosphorylation (pY397) in the tissue specimens of OSCC.

The oncogenic role of androgen receptors in promoting the growth of oral squamous cell carcinoma cells.

Objectives: The aims of this study were to examine the expression of androgen receptors (AR) in oral squamous cell carcinoma (OSCC) cells and tumors and to determine the role of AR in regulating OSCC cell growth.

Materials And Methods: Four OSCC cell lines were used for analyzing AR expression and transcriptional activity. The effects of AR knockdown on the growth and tumorigenicity of OSCC cells were examined.

Regulation of estrogen receptor α function in oral squamous cell carcinoma cells by FAK signaling.

Estrogen receptor α (ERA) is a DNA-binding transcription factor that plays an important role in the regulation of cell growth. Previous studies indicated that the expression of ERα in cell lines and tumors derived from oral squamous cell carcinoma (OSCC). The aim of this study was to examine the activity and function of ERα in OSCC cells and the mechanism underlying ERα activation.

Resveratrol inhibits glucose-induced migration of vascular smooth muscle cells mediated by focal adhesion kinase.

Scope: Diabetes is a critical factor for atherosclerosis, as hyperglycemia induces vascular smooth muscle cell (VSMC) proliferation and migration and subsequently contributes to the formation of atherosclerotic lesions. This study investigates whether resveratrol plays a regulatory role in the proliferation and migration of VSMCs under high glucose induction to imitate a hyperglycemic condition.

Methods And Results: Resveratrol inhibited the migration of VSMCs in the wound-healing assay and the formation of lamellipodia and filopodia as assessed by atomic force microscopy scanning.

Could the excess seen at 124-126 GeV be due to the Randall-Sundrum radion?

Current Higgs boson searches in various channels at the LHC point to an excess at around 124-126 GeV due to a possibly standard-model-like Higgs boson. If one examines more closely the channels (γγ, WW(*), and ZZ(*)) that have excess, this "Higgs boson" may be the Randall-Sundrum radion ϕ. Because of the trace anomaly, the radion has stronger couplings to the photon and gluon pairs.

Heat conduction in chain polymer liquids: molecular dynamics study on the contributions of inter- and intramolecular energy transfer.

In this paper, the molecular mechanisms which determine the thermal conductivity of long chain polymer liquids are discussed, based on the results observed in molecular dynamics simulations. Linear n-alkanes, which are typical polymer molecules, were chosen as the target of our studies. Non-equilibrium molecular dynamics simulations of bulk liquid n-alkanes under a constant temperature gradient were performed.

Antroquinonol inhibits NSCLC proliferation by altering PI3K/mTOR proteins and miRNA expression profiles.

Antroquinonol a derivative of Antrodia camphorata has been reported to have antitumor effects against various cancer cells. However, the effect of antroquinonol on cell signalling and survival pathways in non-small cell lung cancer (NSCLC) cells has not been fully demarcated. Here we report that antroquinonol treatment significantly reduced the proliferation of three NSCLC cells.

Increase of ZASC1 gene copy number in recurrent oral carcinoma.

Backgrounds: The chromosome 3q26 locus is a hotspot region carrying oncogenes that frequently altered in neoplasms. ZASC1 is a zinc finger protein transcription factor localized on 3q26. Our previous study showed the frequent amplification of 3q26, including the ZASC1 gene, in oral squamous cell carcinoma (OSCC).

Next-to-leading-order QCD corrections to the top-quark decay via model-independent flavor-changing neutral-current couplings.

D0 and CDF collaborations at the Fermilab Tevatron have searched for nonstandard-model single top-quark production and have set upper limits on the anomalous top-quark flavor-changing neutral-current (FCNC) couplings kappatcg/Lambda and kappatug/Lambda using the measurement of the total cross section calculated at the next-to-leading order (NLO) in QCD. In this Letter, we report on the effect of anomalous FCNC couplings to various decay branching ratios of the top quark, calculated at the NLO. This result is not only mandatory for a consistent treatment of both the top-quark production and decay via FCNC couplings by D0 and CDF at the Tevatron, but is also important for the study of ATLAS and CMS sensitivity to these anomalous couplings at the CERN LHC.

Mitochondrial redox signaling by p66Shc is involved in regulating androgenic growth stimulation of human prostate cancer cells.

p66Shc is shown to negatively regulate the life span in mice through reactive oxygen species (ROS) production. Recent reports, however, revealed that p66Shc protein level is significantly elevated in several human cancer tissues and growth-stimulated carcinoma cells, suggesting a mitogenic and carcinogenic role for p66Shc. In this communication, we demonstrate for the first time that p66Shc mediates androgenic growth signals in androgen-sensitive human prostate cancer cells through mitochondrial ROS production.

Collider signals of unparticle physics.

Phenomenology of the notion of an unparticle U, recently perceived by Georgi, to describe a scale invariant sector with a nontrivial infrared fixed point at a higher energy scale is explored in details. Behaving like a collection of d(U) (the scale dimension of the unparticle operator O(U)) invisible massless particles, this unparticle can be unveiled by measurements of various energy distributions for the processes Z-->f f U and e- e+-->gammaU at e- e+ colliders, as well as monojet production at hadron colliders. We also study the propagator effects of the unparticle through the Drell-Yan tree-level process and the one-loop muon anomaly.

Neuroendocrine-like prostate cancer cells: neuroendocrine transdifferentiation of prostate adenocarcinoma cells.

Neuroendocrine (NE) cells represent a minor cell population in the epithelial compartment of normal prostate glands and may play a role in regulating the growth and differentiation of normal prostate epithelia. In prostate tumor lesions, the population of NE-like cells, i.e.

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells.

Aberrant regulation in the adhesive ability of cancer cells is closely associated with their metastatic activity. In this study, we examine the role of ErbB-2 in regulating the adhesive ability of androgen receptor (AR)-positive human prostate cancer (PCa) cells, the major cell population of PCa. Utilizing different LNCaP and MDA PCa2b cells as model systems, we found that ErbB-2 activity was correlated with PYK2 activity and adhesive ability in those cells.

Androgen deprivation induces human prostate epithelial neuroendocrine differentiation of androgen-sensitive LNCaP cells.

Neuroendocrine (NE) cells are the minor cell populations in normal prostate epithelial compartments. During prostate carcinogenesis, the number of NE cells in malignant lesions increases, correlating with its tumorigenicity and hormone-refractory growth. It is thus proposed that cancerous NE cells promote prostate cancer (PCa) cell progression and its androgen-independent proliferation, although the origin of the cancerous NE cells is not clear.

Cellular prostatic acid phosphatase: a protein tyrosine phosphatase involved in androgen-independent proliferation of prostate cancer.

Human prostatic acid phosphatase (PAcP) was used as a valuable surrogate marker for monitoring prostate cancer prior to the availability of prostate-specific antigen (PSA). Even though the level of PAcP is increased in the circulation of prostate cancer patients, its intracellular level and activity are greatly diminished in prostate cancer cells. Recent advances in understanding the function of the cellular form of PAcP (cPAcP) have shed some light on its role in prostate carcinogenesis, which may have potential applications for prostate cancer therapy.

Expression of p66(Shc) protein correlates with proliferation of human prostate cancer cells.

p66(Shc), an isoform of Shc adaptor proteins, is shown to mediate various signals, including cellular stress. However, little is known about its involvement in carcinogenesis. We previously showed that p66(Shc) protein level is upregulated by steroid hormones in human carcinoma cells and is higher in prostate cancer (PCa) specimens than adjacent noncancerous cells.