LncRNA PCBP1-AS1 suppresses cell growth in oral squamous cell carcinoma by targeting miR-34c-5p/ZFP36 axis
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Oral squamous cell carcinoma (OSCC) is the most frequently diagnosed oral malignancy and poses a great threat to public health. According to bioinformatics analysis, long noncoding RNA PCBP1-AS1 is downregulated in OSCC. In this work, the functions and mechanism of PCBP1-AS1 in OSCC were further investigated. PCBP1-AS1 expression in OSCC cells was measured by quantitative polymerase chain reaction. Cell viability and proliferation were detected using CCK-8 assays and colony-forming assays. TUNEL assays as well as flow cytometry analyses were carried out to detect OSCC cell apoptosis. Binding relationship between PCBP1-AS1 and miR-34c-5p or that between miR-34c-5p and ZFP36 in OSCC cells was identified using RNA immunoprecipitation assays, RNA pulldown assays, and luciferase reporter assays. Experimental results revealed that PCBP1-AS1 was downregulated in OSCC cells. PCBP1-AS1 overexpression hampered cell proliferation and enhanced cell apoptosis in OSCC. PCBP1-AS1 interacted with miR-34c-5p in OSCC and negatively regulated miR-34c-5p. ZFP36 3'untranslated region was targeted by miR-34c-5p. PCBP1-AS1 positively regulated ZFP36 expression. ZFP36 silencing abrogated the suppressive impact of PCBP1-AS1 on OSCC cell growth. In summary, PCBP1-AS1 suppresses cell growth in OSCC by upregulating ZFP36 through interaction with miR-34c-5p.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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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.
MTT assay
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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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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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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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microRNAs (miRNAs) dysregulation is widely involved in cancer progression and contributed to sustained cell proliferation by directly targeting multiple targets. Therefore, better understanding the underlying mechanism of miRNA in carcinogenesis may improve diagnostic and therapeutic strategies for malignancy. In our study, we found that mir-765 is upregulated in both hepatocellular carcinoma (HCC) cell lines and tissues, compared to human normal liver cell line and adjacent non-cancerous tissues, respectively. Overexpression of mir-765 increased HCC cells proliferation and tumorigenicity, whereas inhibition of mir-765 reverses this effect. Furthermore, we demonstrated that INPP4B as a direct target of mir-765 and ectopic expression of mir-765 repressed INPP4B expression, resulting in upregulation of p-AKT, Cyclin D1, and downregulation of p-FOXO3a, p21 expression in HCC. Strikingly, we found that silencing the expression of INPP4B is the essential biological function of miR-765 during HCC cell proliferation. Collectively, our findings reveal that miR-765 is a potential onco-miR that participates in carcinogenesis of human HCC by suppressing INPP4B expression, and might represent a potential therapeutic target for HCC patients.
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Cyclin E1
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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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