Low shear stress is a component of the tumor microenvironment in vivo and plays a key role in regulating cancer cell migration and invasion. The integrin, as a mechano-sensors mediating and integrating mechanical and chemical signals, induce the adhesion between cells and extracellular matrix (ECM). The purpose of this study is to investigate the effect of low shear stress (1.4 dyn/cm2)on the migration of HepG2 cells and the expression of integrin. Scratch wound migration assay was performed to examine the effect of low shear stress on the migration of HepG2 cells at 0 h, 1 h, 2 h and 4 h, respectively. F-actin staining was used to detect the expression of F-actin in HepG2 cells treated with low shear stress at 2 h and 4 h. Western blot analysis was carried out to determine the effect of low shear stress on the expression of integrin at different durations. The results showed that the migrated distance of HepG2 cells and the expression of F-actin increased significantly compared with the controls. The integrin alpha subunits showed a different time-dependent expression, suggesting that various subunits of integrin exhibit different effects in low shear stress regulating cancer cells migration.
Actins ; physiology ; Cell Movement ; Extracellular Matrix ; physiology ; Hep G2 Cells ; Humans ; Integrins ; physiology ; Stress, Mechanical

OBJECTIVETo study the differences between amelogenesis imperfecta (AI) teeth and normal human (NH) teeth in wear properties.

METHODSThe ultrastructure of the human tooth enamel from adult patient diagnosed with AI was investigated using atomic force microscope (AFM) and compared with the surface of normal human tooth enamel. The composition of tooth enamel of AI teeth and normal human teeth were analyzed by energydispersive X-ray spectroscopy (EDX). The properties of micro-friction and wear between AI teeth and normal human teeth were compared using nano-scratch technology and scanning electron microscope (SEM).

RESULTSThe AI teeth were found porosity and the loosely packed hydroxyapatite was distributed randomly compared with normal human teeth. The amount of C was higher while the amount of Ca, P were lower in AI teeth than normal human teeth. The friction coefficient of both AI teeth and normal human teeth was increasing with the load increased and the friction coefficient of AI teeth was higher than normal human teeth with the same load. Meanwhile, the destruction of AI teeth was more severe than normal human teeth with the same load.

CONCLUSIONThe AI teeth has significant differences with normal human teeth on micro-structure, composition and micro-friction and wear properties. Thus, we need to have a general consideration of all these results when doing clinical restorations.

Adult ; Amelogenesis Imperfecta ; Dental Enamel ; Humans ; Microscopy, Electron, Scanning ; Tooth

Focal adhesion kinase (FAK) plays a critical role in the process of cell adhesion and migration by regulating the expression of downstream small G proteins. A kind of focal adhesion kinase (FAK) inhibitor was used to inhibit the phosphorylation of Y397 site of FAK, and scratch wound migration assay was used to examine the effect of FAK inhibitor with different concentrations (0-250 nmol/mL) on the migration of hepatomal cells (Hep G2 cells) at 0, 2, 4, 8 and 24h. Immunofluorescence analysis and Western blot analysis were performed to detect the expression of F-actin and small G proteins Rac1, RhoA and Cdc42 in Hep G2 cells treated with FAK inhibitor for 120 min. The results indicated that the FAK inhibitor can inhibit the migration of Hep G2 cells with a dose- and time-dependent manner. F-actin was down-regulated in Hep G2 cells treated with FAK inhibitor for 120 min, and expression of small G proteins were inhibited at different durations. The inhibition of FAK phosphorylation could inhibit cell adhesion and migration by down-regulating small G proteins. These results suggested that FAK inhibitor can inhibit the migration of tumor cells by blocking FAK phosphorylation. This means that FAK inhibitor can block the metastasis of tumor cells to surrounding tissues. It may be a potential application in the prevention and treatment of cancer.
Cell Adhesion ; drug effects ; Cell Movement ; drug effects ; Focal Adhesion Protein-Tyrosine Kinases ; antagonists & inhibitors ; metabolism ; physiology ; Hep G2 Cells ; Humans ; Liver Neoplasms ; pathology ; Neoplasm Metastasis ; prevention & control

The article aims to explore the optimal concentration of arsenic trioxide (As O ) on HepG2 of liver cancer cells, and the effect of As O on the migration, invasion and apoptosis of HepG2 cells. In this study, the activity of HepG2 cells treated with 0, 1, 2, 4, 8, 16, 32 μmol/L As O was tested by CCK-8 method, the semi-inhibitory concentration (IC50) was calculated, and the morphological changes of HepG2 cells were observed after the action of As O at IC50 concentration for 12, 24, 48 h. The effect of As O on cell migration and invasion ability was verified by wound healing experiment and Transwell invasion experiment. Western blot and qRT-PCR were used to detect the effects of As O on the gene and protein expression levels related to cell migration, invasion and apoptosis. The results showed that, compared with the control group, the activity of HepG2 cells decreased with the increase of the concentration of As O treatment, showing a dose-dependent effect, and its IC50 was 7.3 μmol/L. After 24 hours' treatment with 8 μmol/L As O , HepG2 cells underwent significant apoptosis, and its migration and invasion abilities were significantly reduced. In addition, the protein expression levels of RhoA, Cdc42, Rac1 and matrix metalloproteinase-9 (MMP-9) were down-regulated, the protein and mRNA expression levels of anti-apoptotic gene Bcl-2 were significantly down-regulated, and the protein and mRNA expression levels of pro-apoptotic genes Bax and Caspase-3 were significantly up-regulated. The above results indicate that certain concentration of As O can inhibit the migration and invasion of hepatocellular carcinoma cells and promote the apoptosis of hepatocellular carcinoma cells.