RNA methyltransferase NSUN2 promotes hypopharyngeal squamous cell carcinoma proliferation and migration by enhancing TEAD1 expression in an m5C-dependent manner
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Cell‐in‐cell structures represent live cell events in which one cell internalizes another. Because formation of cell‐in‐cell structures is a rare event in most cell types and the event is associated with cell death, there has been limited clarification of this phenomenon, and its physiological role and molecular mechanism are yet to be precisely elucidated. In this study, we established a mutagenized cell line that exhibited cell‐in‐cell structures at a more than 10‐fold higher frequency as compared to the parent cells. Interestingly, both engulfment and invasion were increased in the mutagenized cell line as compared with that in the parent cell line in the suspension culture condition. This finding indicates that this mutagenized cell line showed an interchangeable status in terms of its ability to form cell‐in‐cell structures, and the system described here could be useful for elucidation of the mechanisms regulating the formation of cell‐in‐cell structures, including engulfment and invasion, in a given cellular environment. Further studies using this cell line are warranted to understand the mechanism of formation and biological significance of the cell‐in‐cell formation.
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Cell–cell interaction
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Objective To observe the effects of IP6 on human pancreatic adenocarcinoma cell line PC-3 and human pancreatic primary culture cell proliferation and differentiation in vitro.Methods Direct counting cells for cell growth curve,MTT test,flow cytometry test cell apoptosis were used to observe cell proliferation and differentiation.Results IP6 inhibited the growth of human pancreatic adenocarcinoma cell line PC-3 in a time and dose dependent manner.The effect was biggest when the level was 10mmol/L,but little difference with 5mmol/L and 10mmol/L.When less than 5mmol/L,IP6 almost can not effect the growth of human pancreatic primary culture cell;only little inhibition in 5mmol/L,and it was obviously inhibited in 10mmol/L.Conclusion When 5mmol/L,IP6 is the best inhibited density,which could kill tumor cell utmost and interfere normal cell in the lowest level.
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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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Bromodeoxyuridine
Hep G2
Thymidine
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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
Apical cell
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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.
Contact inhibition
Cell Signaling
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Cell Proliferation Profile of Five Human Uveal Melanoma Cell Lines of Different Metastatic Potential
<i>Objective:</i> The aim of this study was to establish a proliferation profile of uveal melanoma cell lines, using different methods, and to compare it with their previously determined metastatic potential (MP). <i>Methods:</i> Four human uveal melanoma and one transformed human uveal melanocytic cell line were ranked according to proliferation profiles. The proliferation profiles of the cell lines were compared to their MPs, which were previously determined from an immunosuppressed rabbit model. <i>Results:</i> Ranking of the cell lines using pulse labeling with tritiated thymidine was similar to the MP of the cell lines. <i>Conclusion:</i> The correlation between the proliferative rate of the uveal melanoma cell lines and their previously determined MP resulted in the proposal of a new classification scheme: high proliferation/high MP, low proliferation/low MP, and high proliferation/no MP. High proliferative capacity of a cell line did not necessarily confer MP; therefore, further cellular functions/adaptations must be required for tumor cell dissemination, survival, and growth at a metastatic site.
Thymidine
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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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Malignant Transformation
Urothelial Cell
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