YAP co-localizes with the mitotic spindle and midbody to safeguard mitotic division in lung-cancer cells.

YES-associated protein (YAP) is a part of the Hippo pathway, with pivotal roles in several developmental processes and dual functionality as both a tumor suppressor and an oncogene. In the present study, we identified YAP activity as a microtubular scaffold protein that maintains the stability of the mitotic spindle and midbody by physically interacting with α-tubulin during mitotic progression. The interaction of YAP and α-tubulin was evident in co-immunoprecipitation assays, as well as observing their co-localization in the microtubular structure of the mitotic spindle and midbody in immunostainings.

Nuclear p120 catenin is a component of the perichromosomal layer and coordinates sister chromatid segregation during mitosis in lung cancer cells.

Abnormal expression of p120 catenin is associated with the malignant phenotype in human lung cancer. Numerous studies have focused on the function of p120 catenin in the juxta-membrane compartment. However, the role of nuclear p120 catenin remains unclear.

Human Caspase 12 Enhances NF-κB Activity through Activation of IKK in Nasopharyngeal Carcinoma Cells.

Human nasopharyngeal carcinoma (NPC) is a highly invasive cancer associated with proinflammation. Caspase-12 (Casp12), an inflammatory caspase, is implicated in the regulation of NF-κB-mediated cellular invasion via the modulation of the IκBα protein in NPC cells. However, the effect mechanisms of Casp12 need to be elucidated.

Downregulation of lumican enhanced mitotic defects and aneuploidy in lung cancer cells.

Lumican is overexpressed in lung cancer cells and has been implicated in the pathogenesis of tumorigenesis and regulation of cancer cell invasion. Lumican is robustly associated with the binding of p120-catenin protein to modulate cell metastasis. However, its role in cancer cell proliferation is still unclear.

Downregulation of lumican accelerates lung cancer cell invasion through p120 catenin.

The overexpression of lumican has been found in lung cancer cells; however, the functional role of lumican in lung cancer cells remains unclear. In this study, we found lumican functioned as a tubulin-binding protein and the depletion of lumican by transfection with its specific shRNA increased lung cancer cell invasion. Such alterations led to morphological changes and actin cytoskeleton remodeling, including the induction of membrane ruffling or protrusion and stress fiber formation, correlated with the increased activities of Rac and Rho.

Caspase 12 degrades IκBα protein and enhances MMP-9 expression in human nasopharyngeal carcinoma cell invasion.

Caspase-12 (Casp12), an inflammatory caspase, functions as a dominant-negative regulator of inflammatory responses and is associated with the signaling of apoptosis. However, the physiological function of Casp12 presented in cancer cells is still unclear. This study demonstrated that overexpression of Casp12 mediated IκBα degradation and significantly increased NF-κB activity.

Interplay of N-Cadherin and matrix metalloproteinase 9 enhances human nasopharyngeal carcinoma cell invasion.

Background: N-cadherin is a trans-membrane adhesion molecule associated with advanced carcinoma progression and poor prognosis. The effect of N-cadherin on matrix metalloproteinase 9 (MMP-9) regulation is implicated in human nasopharyngeal carcinoma (NPC) cell invasion.

Methods And Results: Exposure of NPC cells to phorbol-12-myristate-13-acetate (PMA) or macrophage conditioned media (CM) upregulated MMP-9 and N-cadherin cleavage, which resulted in NPC cell invasion.

Negative pressure induces p120-catenin-dependent adherens junction disassembly in keratinocytes during wound healing.

A negative-pressure of 125mmHg (NP) has been widely used to treat chronic wounds in modern medicine. Keratinocytes under NP treatment have shown accelerated cell movement and decreased E-cadherin expression. However, the molecular mechanism of E-cadherin regulation under NP remains incompletely understood.

Quantifying cell behaviors in negative-pressure induced monolayer cell movement.

Background: Negative-pressure of 125 mmHg (NP) has been shown to accelerate wound healing. Effects of NP on human keratinocyte behaviors during wound healing process were highlighted in this study.

Methods: An NP incubator incorporating the electric cell-substrate impedance sensing (ECIS) technique has been built to quantify monolayer keratinocytes movement in serum-free media at the ambient pressure (AP) and NP for 12 h.

Resveratrol induced ER expansion and ER caspase-mediated apoptosis in human nasopharyngeal carcinoma cells.

Autophagy and endoplasmic reticulum (ER) stress response is important for cancer cells to maintain malignancy and resistance to therapy. trans-Resveratrol (RSV), a non-flavonoid agent, has been shown to induce apoptosis in human nasopharyngeal carcinoma (NPC) cells. In this study, the involvements of tumor-specific ER stress and autophagy in the RSV-mediated apoptosis were investigated.

Negative pressure accelerated monolayer keratinocyte healing involves Cdc42 mediated cell podia formation.

Background: Negative-pressure wound therapy (NPWT) is developed to facilitate wound healing at controlled subatmospheric pressures in modern medicine. Molecular mechanism for this therapy is still undefined.

Objective: This study highlights the localization and time-course of the cell division control protein 42 (Cdc42) in the cell membrane at ambient pressure (AP) and negative pressures of 75mmHg (NP75), 125mmHg (NP125) and 175mmHg (NP175).

Wogonin induces cross-regulation between autophagy and apoptosis via a variety of Akt pathway in human nasopharyngeal carcinoma cells.

Autophagy as well as apoptosis is an emerging target for cancer therapy. Wogonin, a flavonoid compound derived from the traditional Chinese medicine of Huang-Qin, has anticancer activity in many cancer cells including human nasopharyngeal carcinoma (NPC). However, the involvement of autophagy in the wogonin-induced apoptosis of NPC cells was still uninvestigated.

Downregulation of p57kip² promotes cell invasion via LIMK/cofilin pathway in human nasopharyngeal carcinoma cells.

The members of Rho family are well known for their regulation of actin cytoskeleton to control cell migration. The Cip/kip members of cyclin-dependent (CDK) inhibitors have shown to implicate in cell migration and cytoskeletal dynamics. p57(kip2) , a CDK inhibitor, is frequently down-regulated in several malignancy tumors.

Wogonin induced apoptosis in human nasopharyngeal carcinoma cells by targeting GSK-3β and ΔNp63.

Purpose: Wogonin, a plant flavonoid, has antitumor activity in various cancers. Dysregulation of GSK-3β has been implicated in tumorigenesis and cancer progression. In this study, we investigated the antitumor activity and the mechanistic action of wogonin in human nasopharyngeal carcinoma (NPC) cells.

Exercise affects platelet-impeded antitumor cytotoxicity of natural killer cell.

Purpose: Natural killer cells (NK) induce the death of tumor cells by perforin/granzyme-mediated cytotoxicity, whereas platelets reduce the capacity of NK to destroy tumor cells. Physical exercise affects both immune function and platelet activity because responses depend on type, intensity, and duration of exercise. This investigation explores how various exercise regimens influence platelet-impeded cytotoxicity of NK to nasopharyngeal carcinoma cells (NPC).

Overexpression of delta Np63 in a human nasopharyngeal carcinoma cell line downregulates CKIs and enhances cell proliferation.

p63 belongs to a member of the tumor suppressor protein p53 family. Due to alternative promoter usage, two types of p63 proteins are produced. The DeltaNp63 isoform lacks the N-terminal transactivation domain and is thought to antagonize TAp63 and p53 in target gene regulation.

Resveratrol protects vascular endothelial cell from ox-LDL-induced reduction in antithrombogenic activity.

Dietary antioxidants are thought to be beneficial in reducing the incidence of coronary heart disease. In this study, the antithrombogenic endothelial cells (EC) defense was investigated in an experiment model in which cultured endothelial cells were incubated with aggregating platelets in the aggregometer. We examined the possible protective effect of trans-resveratrol (RSV) on oxidized low density lipoprotein (ox-LDL)-induced insults on the antithrombogenic activity of the vascular EC.

Exercise modulates platelet-nasopharyngeal carcinoma cell aggregation and subsequent tissue factor and matrix metalloproteinase activities.

Interaction between platelet and carcinoma cell contributes to pathogenesis of cancer-related thrombosis and metastasis. This study investigated whether physical exercise affects platelet-nasopharyngeal carcinoma cell (NPC) interaction and platelet-promoted tissue factor (TF) and matrix metalloproteinase (MMP) activities of NPC. Thirty sedentary men performed on three occasions moderate-intensity exercise [MIE, 60% maximal oxygen consumption (V(.

Resveratrol attenuates oxLDL-stimulated NADPH oxidase activity and protects endothelial cells from oxidative functional damages.

trans-Resveratrol (RSV) has been shown to have cardioprotective effect during ischemia-reperfusion through reactive oxygen species (ROS)-scavenging activity. Elevated ROS has been implicated in the initiation and progression of atherosclerosis. The nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major source of vascular ROS formation.

Role of exercise intensities in oxidized low-density lipoprotein-mediated redox status of monocyte in men.

Exercise significantly influences the progression of atherosclerosis. Oxidized LDL (ox-LDL), as a stimulator of oxidative stress, facilitates monocyte-related atherogenesis. This study investigates how exercise intensity impacts ox-LDL-mediated redox status of monocytes.

Dual regulation of the DeltaNp63 transcriptional activity by DeltaNp63 in human nasopharyngeal carcinoma cell.

p63 splicing variants lacking NH(2)-terminal transactivating domain, known as DeltaNp63, are thought to antagonize p53 and p63 functions and are suggested to play roles in keratinocyte differentiation. Here, we show that DeltaNp63 has a dual-regulatory effect on the activity of its own promoter in NPC-076 cell. Down-regulation of the transcriptional activity is observed when DeltaNp63 is present in low levels.

Exercise paradoxically modulates oxidized low density lipoprotein-induced adhesion molecules expression and trans-endothelial migration of monocyte in men.

Physical exercise can affect the risk of cardiovascular disease. Oxidized-low density lipoprotein (ox-LDL) promotes transendothelial migration (TEM) of monocyte, thereby accelerating the pathogenesis of atherosclerosis. This study investigated how exercise intensity affects monocyte/EC interactions under ox-LDL-mediated condition.

Antioxidants and myocardial ischemia: reperfusion injuries.

Animal studies have demonstrated that restoration of blood flow to severely ischemic myocardium is a prerequisite for myocardial salvage. However, it has been shown that the restoration of blood flow to ischemic myocardium may be associated with deleterious changes of the myocardium, including arrhythmias, enzyme release, and contractile dysfunction. These changes were considered to be additional injuries to the myocardium manifested at the time of reperfusion.

Effects of exercise training and detraining on oxidized low-density lipoprotein-potentiated platelet function in men.

Objective: To investigate how exercise training and detraining affect oxidized low-density lipoprotein (Ox-LDL)-potentiated platelet function in men.

Design: Cohort study.

Setting: Department of physical medicine and rehabilitation.

Exposure to oxidized low-density lipoprotein reduces activable Ras protein in vascular endothelial cells.

Oxidized low-density lipoprotein (ox-LDL) has been shown to alter the migratory and proliferative activities of the vascular endothelial cells (EC) in response to serum and growth factors. The mechanism underlying the antiproliferative effect of ox-LDL on vascular EC has not been fully elucidated. In this report, we show that exposure of vascular EC to ox-LDL results in a marked reduction of the membrane-associated Ras protein.