ABSTRACT
Aim To study the inhibitory effect of attenuated salmonella SGN1, overexpressing methioninase, on nasopharyngeal carcinoma (NPC) and the underlying mechanism. Methods The cell proliferation, cell cycle, cell apoptosis, clony formation and migration a-bility of 5-8F, HNE-2, CNE-2 cells were measured u-sing flow cytometry assay, clone formation assay, and wound assay after the methionine restriction treatment. 5-8F, HNE-2, CNE-2 cells were infected with SGN1 at the multiplicity of infection (MOI) of 1: 100 for 5 hours, followed with the measurement of cell growth. A xenograft model was constructed by subcutaneous injection of 5-8F cells in mice to observe the inhibitory effect of SGN1 on nasopharyngeal carcinoma. Results Compared with the control group, methionine restriction significantly inhibited the proliferation, migration ability, and clone formation of nasopharyngeal carcinoma cells and blocked the G
ABSTRACT
The 3-D spatial and mechanical features of nano-topography can create alternative environments, which influence cellular response. In this paper, murine fibroblast cells were grown on surfaces characterized by protruding nanotubes. Cells cultured on such nano-structured surface exhibit stronger cellular adhesion compared to control groups, but despite the fact that stronger adhesion is generally believed to promote cell cycle progression, the time cells spend in G1 phase is doubled. This apparent contradiction is solved by confocal microscopy analysis, which shows that the nano-topography inhibits actin stress fiber formation. In turn, this impairs RhoA activation, which is required to suppress the inhibition of cell cycle progression imposed by p21/p27. This finding suggests that the generation of stress fibers, required to impose the homeostatic intracellular tension, rather than cell adhesion/spreading is the limiting factor for cell cycle progression. Indeed, nano-topography could represent a unique tool to inhibit proliferation in adherent well-spread cells.
Subject(s)
Cell Adhesion , Cell Cycle , Fibroblasts/physiology , Nanostructures/chemistry , Animals , Cell Division , Cells, Cultured , Cyclin-Dependent Kinase Inhibitor p21/metabolism , Fibroblasts/cytology , Mice , Tissue Scaffolds , rho GTP-Binding Proteins/metabolism , rhoA GTP-Binding ProteinABSTRACT
In recent years, immunotherapy has been shown to be a promising approach for the treatment of various tumor entities. Due to further pharmacological developments and new studies, the checkpoint inhibitors have now arrived in the clinic. To date, patients with cancers in the head and neck region have benefited from these agents as part of a palliative therapy. Current clinical trials are testing other indications for the checkpoint inhibitors as monotherapy or in combination with other therapeutic approaches. The following article summarizes the highlights of the American Society of Clinical Oncology (ASCO) Annual Meeting.
Subject(s)
Head and Neck Neoplasms , Head and Neck Neoplasms/therapy , Humans , Immunotherapy , Palliative CareABSTRACT
Objective To investigate the apoptosis-inducing effect and anti-proliferative effect of epigallocatechin-3-gallate (EGCG) on human pancreatic cancer cell SW1990 in vitro. Methods The effect of proliferation was evaluated by MTT after the SW1990 cells in vitro were incubated with different concentrations of EGCG (6.25, 12.5, 25, 50, 100 μg/ml). The apoptosis-inducing effect was determined by flow cytometry after the cells were treated with 25 μg/ml of EGCG. The cell cycle of SW1990 cells was detected by flow cytometry after the cells incubated with different concentrations of EGCG (0, 10, 20, 30, 40, 50 μg/ml).Results After SW1990 cell were treated with different concentrations of EGCG (0, 25, 50 μg/ml), the values of A492 were 0.46 ±0.04,0.42 ±0.04,0.27 ±0.03 at 24 h; 0.48 ±0.02, 0.31 ±0.03,0.16 ±0.02at 48 h; 0.51 ±0.01,0.24 ±0.04,0. 14 ±0.04 at 72 h. EGCG inhibited the proliferation of SW1990 in a doseand time-dependant manner(P ＜0.01 ). The apoptotic rates at 24, 48, 72 h were (8.33 ± 1.15 )%, (19.77 ±0.81 )%, (29.17 ± 0.75 )% in the EGCG treatment group; while the corresponding values were (2.77 ±0.45 ) %, (3.20 ± 0.26 ) %, (3.67 ± 0.35 ) % in the control group; and the difference was statistically significant (P ＜0.01 ). After 0, 20, 50 μg/ml of EGCG treatment for 24 h, the percentages of SW1990 cellsin G0/G1 stage were (57.59 ±0.97)%, (62.99 ± 1.91 )%, (68.87 ± 1.88)%, and the percentages of SW1990 cells in G0/G1 stage increased with the increase of concentrations of EGCG, while the percentages of SW1990 cells in G2/M stage decreased with the increase of concentrations of EGCG (P ＜0.01 ). Conclusions EGCG can significantly inhibit the proliferation of SW1990 cells. The mechanism may be related to the apoptosis-inducing effect and the regulation of the cell cycle of the SW1990 cells.