Growth and death in overagitated microcarrier cell cultures
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Abstract The effects of hydrodynamic forces on cell growth are investigated for animal cells growing on microcarriers. A reduction in net growth was observed with high levels of agitation. DNA measurements indicated that the reduction in net growth was due entirely to cell death, from hydrodynamic forces. No inhibition or enhancement of cell replication appeared to occur with high levels of agitation.Keywords:
Microcarrier
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Entosis is a cell-in-cell formation mechanism that targets viable cells for uptake in epithelial cell cultures and human tumors. Entotic cells control their own engulfment, by invading into their hosts in a Rho-GTPase and actomyosin-dependent manner. Although entotic cells are internalized while alive, most eventually undergo a non-apoptotic form of cell death, called entotic cell death, that is executed non-cell-autonomously by autophagy proteins and lysosomes. Here we review the current understanding of entosis and entotic cell death and discuss the potential roles of this process in cancer. Keywords: Cell-in-cell, entosis, entotic cell death, cannibalism, phagocytosis, engulfment, autophagy, LAP, cell competition.
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Cell-in-cell structures are created by one living cell entering another homotypic or heterotypic living cell, which usually leads to the death of the internalized cell, specifically through caspase-dependent cell death (emperitosis) or lysosome-dependent cell death (entosis). Although entosis has attracted great attention, its occurrence is controversial, because one cell line used in its study (MCF-7) is deficient in caspase-3.We investigated this issue using MCF-7 and A431 cell lines, which often display cell-in-cell invasion, and have different levels of caspase-3 expression. Cell-in-cell death morphology, microstructures, and signaling pathways were compared in the two cell lines.Our results confirmed that MCF-7 cells are caspase-3 deficient with a partial deletion in the CASP-3 gene. These cells underwent cell death that lacked typical apoptotic properties after staurosporine treatment, whereas caspase-3-sufficient A431 cells displayed typical apoptosis. The presence of caspase-3 was related neither to the lysosome-dependent nor to the caspase-dependent cell-in-cell death pathway. However, the existence of caspase-3 was associated with a switch from lysosome-dependent cell-in-cell death to the apoptotic cell-in-cell death pathway during entosis. Moreover, cellular hypoxia, mitochondrial swelling, release of cytochrome C, and autophagy were observed in internalized cells during entosis.The occurrence of caspase-independent entosis is not a cell-specific process. In addition, entosis actually represents a cellular self-repair system, functioning through autophagy, to degrade damaged mitochondria resulting from cellular hypoxia in cell-in-cell structures. However, sustained autophagy-associated signal activation, without reduction in cellular hypoxia, eventually leads to lysosome-dependent intracellular cell death.
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Cell fate determination
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To determine the effects of lipotrope modification on breast cancer cell growth and cell death, the human breast cancer cell line MCF-7 was assigned to grow in one of three lipotrope treatment media for four days. The treatment media included lipotrope-control medium (LCM), containing all required lipotropes; lipotrope-deficient medium (LDM), lacking all lipotropes but supplying homocysteine instead; and lipotrope-additive medium (LAM), containing twice as much of each lipotrope as LCM. Cell count and [3H]thymidine incorporation into DNA revealed that LDM slowed cell growth and inhibited cell proliferation in the MCF-7 cell line. Gel electrophoresis showed significant DNA degradation with the appearance of fragments in LDM-treated cells, whereas the DNA in LCM and LAM cells was largely intact. The LDM group displayed more apoptotic bodies as detected by in situ immunohistochemistry. The gene expression level of bcl-2 was lower in cells treated with LDM than in those treated with LCM and LAM, whereas p53 gene expression did not appear different among the three treatment groups. It is concluded that lipotrope deficiency inhibits cell growth and induces programmed cell death in the human breast cancer cell line MCF-7.
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Objective:To study the relationship between the cell density and the cell proliferation phenotype. Methods: Plate clonality assays was used to measure the impact of cell density to cell clonality and cell cycle in BT325、786-0、293、C6 and NIH3T3 cell lines. Results: The clonality decreased when the cells grown to confluence in NIH3T3 and 7860 cell lines respectively.It seem need more cells to decrease the clonality in 293 cell line but there is no relationship between cell density and cell clonality in BT325 and C6 cell lines.Cell cycle analysis show that cell density have no effect on BT325 and C6 but on 786-0、293 and NIH3T3 cell lines. Conclusion: There might exist preventer or preventers,which is proportional to the number of cells,of immortal stem cell to expand.In addition,the rate of stem cell expansion is proportional to that of cell mitosis in immortal cell lines.
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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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Microcarrier
Hep G2
Gamma-glutamyltransferase
Liver cell
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Over the past decades, the increase in maximal cell numbers for the production of mammalian derived biologics has been in a large part due to the development of optimal feeding strategies. Engineering of the cell line is one of probable approaches for increasing cell numbers in bioreactor. We have demonstrated that the over-expression of the c-myc gene in immortalised CHO cells can increase proliferation rate and maximal cell density in batch culture compared to the control. The changes were attributed to a rapid transition into S-phase from a shortened duration of G1 phase and to the uncoupling of cell size from cell proliferation. To achieve the >70% increase in maximal cell density without additional supply of nutrients the cells underwent an overall reduction of 14% in size as well as a significant decrease in glucose and amino acid consumption rate. Consequently, the total biomass accumulation did not show a significant change from the control. The amount of hSEAP-hFc activity of the over expressing c-myc cell line was found to be within 0.7% of the control. It is shown that the manipulation of cell cycle kinetics and indirectly cell metabolism gives higher cell densities in CHO batch cultures. The unaltered apoptotic rate supported the proposition that the increase in cell number was a result of enhance cell cycle kinetics and cellular metabolism rather than increasing viability. Production of hSEAP-hFc from a constitutive c-myc over-expressing cell line did not increase with the increase in cell number.
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