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Siegesbeckia glabrescens (SG) Makino (Compositae) has been used as a traditional medicine for the treatment of allergic and inflammatory diseases. In the present study, we examined the effects and molecular mechanism of the ethanol extract of SG on cell proliferation and invasion in p53 wild-type A549 and p53-deficient H1299 non-small cell lung cancer (NSCLC) cells. SG treatment markedly inhibited the proliferation and invasion in both cell lines, independently of p53 expression. The anti-proliferative effect of SG on A549 cells was mediated by the inactivation of Akt and p70^S6K as evidenced by treatment with LY294002 and rapamycin, respectively. In addition, anti-invasive activity of SG in A549 cells was found to be associated with the inhibition of p70^S6K. In contrast, in H1299 cells the inactivation of p38^MAPK appeared to be involved in SG-mediated inhibition of cell proliferation and invasion. Collectively, these findings suggest that SG modulates cellular fates such as proliferation and invasion by differential regulation of signaling pathways, depending on the status of p53 expression in NSCLC, and support the development of SG as a potent therapeutic agent for the treatment of NSCLC.

Lung cancer is the leading cause of cancer death in the world and classified into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). As tyrosine kinase inhibitors (TKIs), several triterpenoid saponins can target to epidermal growth factor receptor (EGFR), a widely used molecular therapeutic target, to exhibit remarkable anti-proliferative activities in cancer cells. As one of triterpenoid saponins, 20($S$)-ginsenoside Rg3 [20($S$)-Rg3] was confirmed to be an EGFR-TKI in this work. According to the quantitative real-time reverse transcription-PCR (qRT-PCR) and immunoblotting analysis, 20($S$)-Rg3 was certified to play a key role on EGFR/Ras/Raf/MEK/ERK signal pathway regulation. Our data demonstrated that 20($S$)-Rg3 might block the cell cycle at the G0/G1 phase by downregulating CDK2, Cyclin A2, and Cyclin E1. Molecular docking suggested that the combination of both hydrophobic and hydrogen-bonding interactions may help stabilizing the 20($S$)-Rg3-EGFR binding. Furthermore, their binding stability was assessed by molecular dynamics simulation. Taken together, these data provide the evidence that 20($S$)-Rg3 could prohibit A549 cell proliferation, probably by arresting the cell cycle at the G0/G1 phase via the EGFR/Ras/Raf/MEK/ERK pathway.

The in vitro and in vivo biocompatibility of the ZnO nanoparticles were evaluated using cell model and animal model, by MTT assay, flow cell cytometry, pathological optical and electron microscopy examinations. Both the L929 cell and Hela cell proliferative activity were strongly inhibited by the presence of ZnO nanoparticles, no matter cultured with low dose and high dose suspension. AnnexinV-FITC/PI-FCM assay showed that the number of necrotic cell and apoptotic cell increased significantly. Feeding the ZnO nanoparticle suspension through digestive tract would lead to the damage to some primary organs (heart, lung, liver and kidney). Further investigation by TEM showed the expanded sarcoplasmic reticulum and organelle vacuolation features.

A SiC coating for carbon/carbon (C/C) composites was produced by pack cementation to use as a bonding and buffer layer between C/C composites and bioactive ceramic for application in orthopaedic implants. The microstructure and MG63 osteoblast-like cell responses of the coating were investigated. The results confirmed that the SiC coating displayed a dense and uniform microstructure. MG63 cells attached and spread favorably on SiC coating, and cell proliferation was better on SiC coating than on uncoated C/C composites surface. The SiC coated C/C composites have the potential to be used in artificial implants.

One of the most challenging problems in muscular skeletal trauma is the limited capacity of regeneration of the damaged skeletal muscle fibers after injury and the inevitable replacement by fast growing fibrous tissue compromising function. To date, there is no effective therapeutic measure available in clinical practice. In the present study, red skeletal muscle aqueous extract has been prepared from female adult rats. This muscle extract could strikingly trigger the proliferation and differentiation of myoblasts whose progeny subsequently fuse to preexisting partially damaged muscle fibers to repair the damaged muscle fibers or to form new myotubes to replace the completely damaged muscle fibers during the process of muscle healing and regeneration in vivo. The active myogenic components are probably polypeptides since trypsin or heat treatment could abolish their activity in myogenesis.

Cytoskeleton plays a central role in many cellular processes, such as migration, adhesion and proliferation. Alterations of its structural properties are commonly associated with different diseases (malignancy, cardiac hypertrophy, etc.). In this work, we studied the effects of X-radiations on cytoskeleton architecture of two cell lines: BALBc/3T3 and Simian virus 40-transformed BALBc/3T3 (SVT2) cells. In agreement with the current literature, we observed reduced adhesion and increased motility of SVT2 cells respect to non-transformed BALBc/3T3. In addition, we showed that two different doses of X-rays (1 and 2 Gy) increased cell-dish adhesiveness and reduced cell proliferation and cell motility of transformed cells, whereas minor effects were measured on the normal counterpart. These results suggested that low doses or fractioning of X-rays may have a normalization effect on the investigated parameters for the transformed cell phenotype.

The low-intensity ultrasound effects on MCF7 (human breast adenocarcinoma) and MCF10A (healthy breast cells) have been investigated at different sonication protocol to probe the effectiveness and the selectivity of the ultrasound (US) treatment and to understand the implications between cell mortality, biomechanical interactions and cell elastic modulus. Experiments performed at fixed and variable frequency demonstrated the effectiveness of some protocols in killing carcinogenic cells and the healthy cells insensitivity. Variation of elastic properties of MCF7 cells exposed to US under varying sonication conditions was examined. Sonication was carried out at fixed frequency (as it is usually done in therapy protocols), between 400kHz and 620kHz, following two protocols: (i) at fixed power output; (ii) at fixed voltage of the US generator. Evolution of cell stiffness during the US treatment was monitored via atomic force spectroscopy (AFS). It was found that cell mortality has a similar trend of variation with respect to sonication frequency regardless of the way specimens are exposed to US. Mechanical properties do not show a uniform trend with respect to frequency, but variations of Young’s modulus are more marked near the very low (400–480) kHz or very high frequencies (580–620) kHz. The observed variations may be related to mechanical interactions occurring in the cell culture, suggesting a primacy of the environment on other factors.

A new mathematical model of chronic hepatitis C virus (HCV) infection incorporating humoral and cell-mediated immune responses, distinct cell proliferation rates for both uninfected and infected hepatocytes, and antiviral treatment all at once, is formulated and analyzed meticulously. Analysis of the model elucidates the existence of multiple equilibrium states. Moreover, the model has a locally asymptotically stable disease-free equilibrium (DFE) whenever the basic reproduction number is less than unity. Local sensitivity analysis (LSA) result exhibits that the most influential (negatively sensitive) parameters on the epidemic threshold are the drug efficacy of blocking virus production and the drug efficacy of removing infection. However, LSA does not accurately assess uncertainty and sensitivity in the system and may mislead us since by default this technique holds all other parameters fixed at baseline values. To overcome this pitfall, one of the most robust and efficient global sensitivity analysis (GSA) methods, which is Latin hypercube sampling-partial rank correlation coefficient technique, elucidates that the proliferation rate of infected hepatocytes and the drug efficacy of killing infected hepatocytes are highly sensitive parameters that affect the transmission dynamics of HCV in any population. Our study suggests that cell proliferation of the infected hepatocytes can be very crucial in controlling disease outbreak. Thus, a future HCV drug that boosts cell-mediated immune response is expected to be quite effective in controlling disease outbreak.

This work reports the effects of introducing diverse chemical functionalities onto the surface of polystyrene microcarrier beads on their ability to function as injectable cell carriers. Cellular adhesion and proliferation, as well as cellular outgrowths from microcarrier surfaces, using human umbilical vein endothelial cells (HUVECs), were examined in detail. It was observed that initial cell adhesion appeared to be most significantly decreased by hydrophobicity, whilst cell proliferation appeared to be improved in most chemical functional groups over unmodified polystyrene. Overall, our study highlights the importance of surface chemistry in directing the growth and function of human endothelial cells.

Electricity has been shown to exhibit significant effects on immunological responses in many studies. In this study, an electrostatic filed induced device was first applied to the macrophage cell culturing process. Mouse macrophage-like cells J774 A.1 were exposed to the electrostatic field of 1.5 kV for 1, 2, and 6 days, respectively. The results show that the electrostatic field can inhibit cell proliferation and TNF-α secretion in six days. Cell proliferation is decreased and TNF-α secretion is increased with increasing voltage applied from 0 kV to 0.8 kV and 1.2 kV of the electrostatic fields.

To observe the effect of Polysaccharides from Platycodonis Radix (PRPS) on the rat airway smooth muscle cells (ASMCs) proliferation in vitro. Methods: ASMCs were obtained from adult SD rats by trypsin-collagenase digestion method. In vivo experiment, the cells proliferating model of rat ASMCs were established by ET-1 and the intervention of PRPS. ASMCs were treated with PRPS at different concentrations and the growth of the cells was analyzed by MTT assay. The expression of PCNA in cells was detected by immunocytochemical method. Results: At the end of the experiment, the growth curve of high dosage group of PRPS was significantly lower than that in the model group (0.1521±0.0053). The expression of PCNA in this group was also lower than the model group and slightly higher in the dexamethasone treated group. Conclusion: PRPS can inhibit the proliferation of ASMCs induced by endothelin-1 in vitro, the mechanism has correlation with down- regulation of the expression and PCNA.