Biological gel-based microchamber array for tumor cell proliferation and migration studies in well-controlled biochemical gradients
Jingru YaoGuoqiang LiYang JiaoYu ZhengYanping LiuGao WangLianjie ZhouHongfei ZhangXianquan ZhangJianwei ShuaiQihui FanFangfu YeSilong LouChen GuoKena SongYong LiaoLiyu Liu
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A microchamber array with composite ECM device enables the construction of a more realistic model for investigating cancer migration mechanisms and has potential to serve as a platform for personalized medicine screening.Objective To investigate the effects of simulated weightlessness on cell proliferation and cell cycle of human gastric carcinoma cell line SGC-7901 and human gastric mucosa cell line HFE-145. Methods A rotating clinostat was used to simulate weightlessness. Every cell line was divided into two groups, one was rotating group, the other was 1G control group. The whole experimental session was 72h. The expressions of PCNA(proliferating cell nuclear antigen) were examined by immunohistochemical stain. The changes of cell cycle were examined by a cytometer. Results Compared with the control group, the cell proliferation of SGC-7901 cell was inhibited in 48h and 72h in the rotating group, and the cell conversion from G1 to S phase was suppressed. Compared with the control group, the cell proliferation of HFE-145 cell was inhibited in 12h in the rotating group, and the cell conversion from G1 to S phase was suppressed. Conclusions the cell proliferation of SGC-7901 cell is inhibited in 48h and 72h during simulated weightlessness by a clinostat, but HFE-145 cells only have present those above-mentioned changes in 12h during simulated weightlessness by a clinostat.
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Weightlessness
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Significance Cell–cell contact-mediated responses play a key role in coordinating cell migration. The conventional view has emphasized repulsive responses, based primarily on studies of head-on collisions. Using micropatterned substrates to facilitate various modes of collision, we report that cells migrate toward their neighbors upon contact with tails. This response, referred to as contact following of locomotion (CFL), is found with both epithelial and mesenchymal cells and is reminiscent of the behavior of Dictyostelium discoideum during stream formation. Pharmacological studies implicate the Wnt signaling pathway, and suggest that CFL is necessary for collective migration. CFL may thus represent a critical aspect of diverse biological phenomena that involve collective migration, such as wound healing, tissue development, and metastasis.
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Objective:To study the effected of berberine on cell proliferation,cell cycle and CD44V6 expression in gastric cancer cell(MGC-803).To investigate the mechanism of inhibitory tumor proliferation and tumor metastasis.Methods:MTT assay was used to determine the cell proliferation effected by berberine.The change of cell morphology and cell cycle were detected by laser scanning confocal microscope(LSCM) and flow cytometry,respectively.Immunohistochemical staining and flow cytometry were applied to detect the CD44V6 expression on cell surface.Results:It was found that the proliferation of MCG-803 is inhibited by berberine.The inhibitory rate of drug(10、20、40 μg/ml)is 36 2%、49 7% and 59 3% respectively in a dose-dependent manner.The cell nuclear condensation and formation of apoptotic bodies were found under LSCM.The cell cycle were arrested in G0-G1.The expression of CD44V6 on cell surface was obviously decreased.Conclusion:Berberine could inhibit proliferation of MGC-03 by inducing apoptosis and arresting cell in G0-G1.Berberine could inhibit tumor metastasis by decreasing the expression of CD44V6 on MCG-803.
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Objective: To observe the effects of total saponins and total polysaccharides extracted from shenmai on the proliferation and migration of vascularendothelial cell.Methods: The effects of total saponins and total polysaccharides from shenmai on the proliferation of ECV-304 cell and gastric carcinoma SGC-7901 as well as ECV-304 cell induced by SGC-7901 cell were measured by MTT colorimetric assay.Their effects on the migration of ECV-304 cell were investigated by agaros assay.Results: When the concentration of total polysaccharides from shenmai was in the range of 0.18～2.88mg/mL,there was no influence on the proliferation of ECV-304 cell and gastric carcinoma SGC-7901 as well as ECV-304 cell induced by SGC-7901 cell when the concentration of total saponins from shenmai was in the range of 0.05～0.8mg/mL,there was no influence on the proliferation of(SGC-)7901 cell,but they were able to inhibit the proliferation of ECV-304 cell and ECV-304 cell induced by SGC-7901 cell.The inhibition was(13.16)%～62.77%.There was no influence of total polysaccharides from shenmai on the migration of ECV-304 cell,but total saponins from shenmai can inhibit the migration of ECV-304 cell.The inhibition was 42%～80%.The compounds of total saponins and total asragalans from shenmai can also inhibit the proliferation and migration of vascularendothelial cell,there were no difference between the compounds and total polysaccharides in statistics.Conclusion:Total saponins from shenmai can inhibit the proliferation of vascularendothelial cell and vascularendothelial cell induced by conditional cultured medium of gastric carcinoma cell,they also can inhibit the migration of vascularendothelial cell.Total saponins from shenmai are active compounds.
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Summary: Determinate growth of leaves means that the number and size of their constituent cells must be preciselycontrolled in order to develop to a reproducible size. In the past few years, many mutants and genes involved in the control of cell proliferation and cell expansion in leaves have been identified. In addition, several mutants show an intriguing phenomenon, known as compensated cell enlargement where the reduced number of leaf cells triggers excess cell expansion in leaves. This phenomenon suggests that there is a regulatory system that coordinate cell proliferation and cell expansion. In this review we summarize current knowledge concerning the regulation of cell proliferation and cell expansion and discuss possible mechanisms for compensated cell enlargement. Arabidopsis thaliana, Cell expansion, Cell proliferation, Compensated cell enlargement
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The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. Furthermore, halting and resuming proliferation results in the synchronized response of cell migration on the villi. We conclude that cell proliferation within the crypt is the primary force that drives cell migration along the villus. This methodology can be applied to interrogate intestinal epithelial dynamics and characterize situations in which processes involved in cell turnover become uncoupled, including pharmacological treatments and disease models.—Parker, A., Maclaren, O. J., Fletcher, A. G., Muraro, D., Kreuzaler, P. A., Byrne, H. M., Maini, P. K., Watson, A. J. M., Pin, C. Cell proliferation within small intestinal crypts is the principal driving force for cell migration on villi. FASEB J. 31, 636–649 (2017). www.fasebj.org
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We report a novel mechanism of cellular growth control. Increasing the density of endothelial or smooth muscle cells in culture increased cell‐cell contact and decreased cell spreading, leading to growth arrest. Using a new method to independently control cell‐cell contact and cell spreading, we found that introducing cell‐cell contact positively regulates proliferation, but that contact‐mediated proliferation can be masked by changes in cell spreading: Round cells with many contacts proliferated less than spread cells with none. Physically blocking cell‐cell contact or inhibiting PI3K signaling abrogated cell‐cell induced proliferation, but inhibiting diffusible paracrine signaling did not. Thus, direct cell‐cell contact induces proliferation in these cells.
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Cell Signaling
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Objective To investigate the suppressive effect of Resverol(Res) on proliferation of C6 cell. Methods Res at various concentrations were used to process the C6 cell; the inhibitory action on the growth of C6 cell was evaluated through MTT assay. The cell cycle distribution change and apoptosis induced by Res were examined through flow cytometer (FCM). In addition, the electron microscope was applied to observe the change of the cell's ultra microstructure. Results The experiment showed that Res could suppress the growth and multiplication of C6 cell in a doesand time-dependent manner. Simultaneously Res could effect the C6 cell's cycle distribution, block the cell advancing from G1 to S period. In the experiment the C6 cell apoptosis was induced by Res and the ultra microstructure of C6 cell changed. Conclusion Res obviously suppressed the proliferation of C6 cell and induced its apoptosis and change the cell cycle.
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Cell migration plays a vital role in carcinoma invasion and metastasis. Cell regulatory volume decrease (RVD), a mechanism of adjusting cell volume, is a basic physiological function of cells, which is closely related to cell migration. In this work, a quartz crystal microbalance (QCM) cytosensor was first developed for real-time monitoring of cell RVD to evaluate the migration of human breast cancer cells. While stimulating the immobilized cells on the chip with hypotonic solutions, the temporal dynamics of RVD can be tracked by QCM sensor via analyzing frequency shifts during the cell swelling and shrinkage. The results showed that, due to the difference in cell migration capability, the level of RVD for MCF-7 cells and MDA-MB-231 cells was 32.8 ± 2.9% and 49.7 ± 4.2% ( n = 3), respectively. Furthermore, tamoxifen, a chloride channel blocker, was used to suppress cell RVD, indicating concentration dependence and inhibition difference in both types of cells. Combining QCM measurement with cell migration assay, the results showed that the blockage of RVD was positively correlated to the inhibition of cell migration with tamoxifen concentration ranging from 5 to 60 μM, which revealed the relation between cell RVD and cell migration. The study provided a noninvasive and real-time strategy for monitoring cell RVD as well as assessing cell migration, which was expected to supply a new diagnostic tool for metastatic cancers.
Quartz Crystal Microbalance
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