OBJECTIVETo explore the effect of quercetin on the invasion, migration, proliferation and cell cycle of glioma U87 cells.

METHODSGlioma U87 cells were treated with 50, 100, or 150 µmol/L quercetin (Q(50), Q(100) and Q(150) groups, respectively) or with DMSO (Q(0) group). Transwell in vitro invasion and migration assays, Click-iT Edu test and flow cytometry were performed to evaluate the effect of quercetin on the invasion, migration, proliferation and cell cycle of U87 cells.

RESULTSAfter 36 h of quercetin treatment, the cells in Q(50), Q(100) and Q(150) groups showed invasive cell percentages (relative to Q(0) group) of 52.08%, 24.63%, and 13.13%, respectively (P<0.05). After quercetin treatment for 12 h, the migrating cell percentages (relative to Q(0) group) in Q(50), Q(100) and Q(150) groups were 49.46%, 26.78%, and 14.56%, respectively (P<0.05). After 24 h of quercetin treatment, the cell proliferation ratios in Q(0), Q(50), Q(100) and Q(150) groups were 25.21%, 18.38%, 16.74% and 15.24%; the cell percentages in phase G0/Gl were 71.14%, 72.71%, 69.29%, and 66.47%, phase S were 25.32%, 22.48%, 21.96%, and 23.32%, and phase G(2)/M were 3.53%, 4.80%, 8.75%, and 10.25% in the 4 groups, respectively, showing a significant difference between groups Q(100), Q(150) and group Q(0) in phase G(2)/M cell percentages (P<0.05).

CONCLUSIONSQuercetin can significantly inhibit the invasion, migration and proliferation of glioma U87 cells by blocking the cell cycle progression.

Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Glioma ; pathology ; Humans ; Quercetin ; pharmacology

BACKGROUNDBisphosphonates (BPs) have been reported to reduce local recurrence in giant cell tumor (GCT) of bone because of their osteoclast-suppressing effect; however, the optimal mode of delivery and the dose and duration of treatment of BPs remain to be established. To address these issues, it is first necessary to clarify the manner of action of BPs on osteoclasts. We herein evaluated the osteoclast-suppressing effect of sodium ibandronate in vitro.

METHODSMouse osteoclasts (OCLs) were generated in vitro using mouse bone marrow mononuclear cells. First, various concentrations of sodium ibandronate and equal amounts of phosphate-buffered saline were added to cell culture media. The number of multinucleated cells (over three nuclei) was recorded in each group, OCL formation was compared, and the most effective concentration of sodium ibandronate was determined. Then, high concentrations of sodium ibandronate were added to the experimental cell culture media; no ibandronate was given in the control group. Comparisons were made between the two groups in terms of OCL adhesion, migration, and bone resorption.

RESULTSOCL formation was suppressed by sodium ibandronate in vitro; the most pronounced effect was observed at the concentration of 10(-5) mol/L. OCL migration and bone resorption were significantly suppressed at this concentration, though there was no effect on OCL adhesion.

CONCLUSIONSSodium ibandronate was effective in suppressing OCLs and decreasing resorption in GCT. The strong anti-OCL effectiveness at a high concentration in vitro indicates a topical mode of application.

Animals ; Bone Resorption ; Cell Movement ; drug effects ; Cells, Cultured ; Diphosphonates ; pharmacology ; Mice ; Osteoclasts ; cytology ; drug effects

Chitosan is a natural biopolymer and is made up of D-glucosamine subunits linked by beta-(1,4) glycosidic bond. In recent years, the application of chitosan has attracted more and more attention because of its good biological function in cell biology. The properties of chitosan-based biomaterial are attributed to the physical properties and chemical composition of chitosan. The author of this paper summarized recent related studies and progresses of the influence of physical properties of chitosan on cell activity and cell mechanics property at home and abroad. The findings show that most studies mainly focused on the influence of chitosan and cell activity, while few were on cell mechanics property. The related studies of the influence of chitosan on cell will contribute to the explanation for the mechanism of the interaction between chitosan and cell, and provide the theoretical support for the further study.
Animals ; Cell Adhesion ; drug effects ; Cell Differentiation ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Chemical Phenomena ; Chitosan ; chemistry ; pharmacology ; Humans ; Tissue Engineering ; Tissue Scaffolds ; chemistry

Emodin has such pharmacological effects as ant-inflammatory, anti-tumor, immunoregulation. Meanwhile, emodin could be used for inhibiting the proliferation of vascular smooth muscle cells (VSMC). Many foreign studies demonstrated that emodin had an effect on inhibiting proliferation of VSMCs and cell migration and promoting cell apoptosis, and probed into molecular mechanisms in all aspects. Besides, clinical translational researches and application explorations were also carried out. This article summarizes the research progress of the anti-proliferation effect of emodin on VSMCs.
Apoptosis ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Emodin ; pharmacology ; Humans ; Muscle, Smooth, Vascular ; cytology ; drug effects ; metabolism ; Signal Transduction ; drug effects

To improve the function of endothelial progenitor cells (EPCs) is one of the goals in Chinese traditional therapy to treat various cardio-celebrovascular diseases. In the past decades, scholars in the field of traditional Chinese medicine (TCM) have found fifteen active compounds to regulate the function of EPC. These metabolites are extracted from thirteen, plant-based Chinese medicine, with majority of them as potent reductive or oxidative hydrophilic molecules containing phenyl groups. These active compounds either enhance the mobilization of EPC, or inhibit their apoptosis through different signaling pathways. In this review, the molecular structure, biophysical properties, and the plant sources of these active ingredients and their regulatory effects on the function of EPC are summarized, aiming to reveal the modern basis of Chinese medicine for promoting blood circulation and removing blood stasis at the progenitor cell level.
Animals ; Apoptosis ; drug effects ; Cell Movement ; drug effects ; Cell Survival ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Endothelial Progenitor Cells ; cytology ; drug effects ; metabolism ; Humans ; Signal Transduction ; drug effects

OBJECTIVEThe renal disease is commonly associated with hyperlipidemia and correlates with glomerular accumulation of atherogenic lipoproteins and mesangial hypercellularity. Therefore, in this study, the authors investigated a possible growth stimulatory effect and mode of action of lipoprotein(a) [Lp(a)] in human mesangial cells HMC, and the effect of Lp(a) on adhesion and migration in human mesangial cells.

METHODSThe DNA synthesis of HMC was measured by (3)H-thymidine incorporation. The cell adhesion was detected by the expression of vinculin by means of indirect immunofluorescence. The cell migration was observed under the microscope.

RESULTSThe incubation of HMC with Lp(a) for 24 hours induced a significant dose-dependent proliferation of HMC [Lp(a): 5 microg, 10 microg, 25 microg, 50 microg/ml vs. control 0 microg/ml; (3)H-TdR incorporation (x 10(3)cpm): 1.69 +/- 0.48, 3.59 +/- 0.68, 4.14 +/- 0.78, 4.05 +/- 0.55 vs. 1.64 +/- 0.31, P < 0.01]. The vinculin staining by indirect immunofluorescence showed positive result when HMC was incubated with 10 microg/ml Lp(a) for 24 hours, while vinculin was negative when HMC was incubated with 0 microg/ml Lp(a) as the control of the study. The incubation of HMC with 10 microg/ml Lp(a) for 72 hours demonstrated significant cell migration effect compared to the control of 0 microg/ml. (16.2/LP vs. 2.4/LP, P < 0.01).

CONCLUSIONLp(a) could stimulate a proliferation, adhesion and migration effect on human mesangial cells.

Cell Adhesion ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Intercellular Signaling Peptides and Proteins ; pharmacology ; Lipoprotein(a) ; pharmacology ; Mesangial Cells ; drug effects

OBJECTIVE: To investigate the effect and mechanism of tea polyphenol (TP) on the proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma(NPC) cell line HONEl. METHOD: After treated with different concentration of tea polyphenol, CCK-8 assay, fluorescent staining, cell scratching assay and transwell assay were applied to detect the effect of tea polyphenol on the HONE1 cells. Furthermore, the expression of protein VEGF was investigated by flow cytometry assay. RESULT: It was found that tea polyphenol could inhibit NPC cell proliferation significantly in a dose-dependent manner, however, little impact was observed in normal nasopharyngeal epithelial cell line NP69. Furthermore, it was demonstrated by fluorescent staining assay that tea polyphenol could induce NPC cell apoptosis, and cell scratching assay and transwell assay showed that tea polyphenol could inhibit cell migration and invasion. CONCLUSION Tea polyphenol can significantly inhibit cell proliferation, induce cell apoptosis and decreased the migration and invasion ability of NPC cells in vitro. Tea polyphenol might be a tumor suppressor of NPC cells.
Apoptosis ; drug effects ; Carcinoma ; Cell Line, Tumor ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; pathology ; Polyphenols ; pharmacology ; Tea ; chemistry

AIMTo assess whether exogenous estradiol has any effect on migration of primordial germ cells (PGCs) in the chick.

METHODSFertilized eggs were treated with 17beta-estradiol (E(2)) (80 microg/egg) at stage X (day 0 of incubation), stages 8-10 (incubation 30 h) and 13-15 (incubation 55 h). Controls received vehicle (emulsion) only. Changes in PGC number were measured on different days according to developmental stages.

RESULTSIn male right gonads, but not in female left gonads, at stages 28-30 (incubation 132 h) significant decreases in the mean number of PGCs aggregating were observed compared with the controls (P < 0.05) while the total PGC number in the right and left gonads at each stage did not change (P > 0.05).

CONCLUSIONThe present study provides evidence that E(2) has significant effects on the localization of PGCs in male right, but not female left, gonads of chicken embryos at stages 28-30, compared with controls.

Animals ; Cell Movement ; drug effects ; Chick Embryo ; Estradiol ; pharmacology ; Female ; Germ Cells ; drug effects ; Gonads ; drug effects ; Male

Endothelial progenitor cells (EPCs) play an important role in diabetic vascular complications. A large number of studies have revealed that some clinical antihyperglycemics can improve the complications of diabetes by regulating the function of EPCs. Metformin can improve EPCs function in diabetic patients by regulating oxidative stress level or downstream signaling pathway of adenosine monophosphate activated protein kinase; Pioglitazone can delay the aging of EPCs by regulating telomerase activity; acarbose, sitagliptin and insulin can promote the proliferation, migration and adhesion of EPCs. In addition to lowering blood glucose, the effects of antihyperglycemics on EPCs may also be one of the mechanisms to improve the complications of diabetes. This article reviews the research progress on the regulation of EPC proliferation and function by antihyperglycemics.
Cell Movement/drug effects* ; Cells, Cultured ; Endothelial Progenitor Cells/drug effects* ; Humans ; Hypoglycemic Agents/pharmacology* ; Signal Transduction/drug effects*

OBJECTIVETo study the influence of histatin 1 (Hst1) on the proliferation and migration of human epidermal cell line HaCaT.

METHODS(1) HaCaT cells were routinely cultured and divided into control group, 100, 30, and 3 µg/mL Hst1 groups, 10 ng/mL recombinant human epidermal growth factor (rhEGF) group, and 30 µg/mL Hst1 + 10 ng/mL rhEGF group, according to the random number table (the same dividing method used for following grouping), with 27 samples in each group. NO stimulating factor was added in control group, while Hst1 and(or) rhEGF in corresponding concentration(s) was (were) added in the latter 5 groups. Cell proliferation was assayed by cell counting method at post culture hour (PCH) 24, 48, and 72. (2) HaCaT cells were divided into control group and 100, 30, and 3 µg/mL Hst1 groups, with 27 samples in each group. NO stimulating factor was added in control group, while Hst1 in corresponding concentration was added in the latter 3 groups. Cell cycle was assayed with flow cytometry at PCH 24, 48, and 72, and PI was calculated. (3) HaCaT cells were divided into control group, 30 µg/mL Hst1 group, 10 ng/mL rhEGF group, 30 µg/mL Hst1 + 10 ng/mL rhEGF group, 15 µg/mL Hst1 + 5 ng/mL rhEGF group, and 15 µg/mL Hst1 + 10 ng/mL rhEGF group, with 10 samples in each group. NO stimulating factor was added in control group, while Hst1 and(or) rhEGF in corresponding concentration(s) was (were) added in the latter 5 groups. Cells in each group were divided into two portions: cells in one portion were treated by mitomycin C for 2 hours, while cells in the other portion were not. Scratching assay was conducted in both portions of cells. Cell migration was measured at post scratching hour (PSH) 0, 16, and 24, and the wound-area healing rate was calculated. Data were processed with analysis of variance, and LSD- t test or Dunnett t test was applied in paired comparison among groups.

RESULTS(1) At PCH 24, the cell numbers in 10 ng/mL rhEGF group and 30 µg/mL Hst1 + 10 ng/mL rhEGF group were significantly higher than that in control group (with t values respectively 3.813, 5.410, P < 0.05 or P < 0.01). Except for cell numbers in 30 µg/mL Hst1 group and 3 µg/mL Hst1 group at PCH 48, cell numbers in the other groups as treated by Hst1 and (or) rhEGF were significantly higher than those in control group at PCH 48 and 72 (with t values from 7.754 to 24.979, P values all below 0.01). At PCH 72, the cell number was obviously higher in 100 µg/mL Hst1 group [(19.21 ± 0.59)×10⁴] than in 30 µg/mL Hst1 group [(16.19 ± 0.53)×10⁴)] and 3 µg/mL Hst1 group [(15.38 ± 0.13)×10⁴], with t values respectively 11.391, 19.017, P values all below 0.01. The cell number was higher in 30 µg/mL Hst1 + 10 ng/mL rhEGF group than in 30 µg/mL Hst1 group, 3 µg/mL Hst1 group, and 10 ng/mL rhEGF group (with t values from 4.579 to 34.884, P < 0.05 or P < 0.01). Cell numbers in all groups increased with prolongation of time. (2) Compared with those in control group at PCH 24 and 48, the percentage of cells in G0/G1 phase was decreased, the percentage of cells in S phase was increased (except for cell percentage of 30 µg/mL Hst1 group at PCH 24), and PI value was significantly increased in 100 µg/mL Hst1 group and 30 µg/mL Hst1 group (with t values from 4.752 to 16.104, P values all below 0.01). The PI value in 3 µg/mL Hst1 group was obviously higher than that in control group only at PCH 48 (t = 4.609, P < 0.01). At PCH 72, only the PI value in 100 µg/mL Hst1 group was higher than that in control group (t = 8.005, P < 0.01). Compared among the groups treated by Hst1, the percentage of cells in G0/G1 phase showed an elevating trend, and the percentage of cells in S phase and the PI value showed a declining trend along with the decrease in Hst1 concentration at each time point. Compared within each group treated by Hst1, the percentage of cells in G0/G1 phase declined first and then elevated, while the percentage of cells in S phase and the PI value elevated first and then declined along with prolongation of time. (3) Without treatment of mitomycin C, the wound-area healing rate in 30 µg/mL Hst1 group (75.9 ± 3.9)% at PSH 16 was significantly higher than those in control group and 10 ng/mL rhEGF group [(53.0 ± 3.5)%, (61.7 ± 2.5)%, with t values respectively 12.241, 7.598, P values all below 0.01], but lower than those in 30 µg/mL Hst1 + 10 ng/mL rhEGF group, 15 µg/mL Hst1 + 5 ng/mL rhEGF group, and 15 µg/mL Hst1 + 10 ng/mL rhEGF group [(95.0 ± 4.1)%, (97.0 ± 3.7)%, (80.5 ± 5.9)%, with t values from -11.324 to -2.502, P < 0.05 or P < 0.01]. After being treated by mitomycin C, the wound-area healing rate in 30 µg/mL Hst1 group at PSH 16 [(54.1 ± 4.5)%] was higher than that in control group [(35.8 ± 5.7)%, t = 7.790, P < 0.01], but lower than that in the same Hst1 concentration but without mitomycin C treatment group (t = -10.863, P < 0.01). There was no statistically significant difference in the wound-area healing rate between 30 µg/mL Hst1 group and other groups treated by Hst1 and rhEGF at PSH 16 (with t values from 0.061 to 2.030, P values all above 0.05). Compared within each group with or without treatment of mitomycin C, the wound-area healing rate at PSH 16 was not significantly different from that at PSH 24 (with F values from 0.856 to 3.062, P values all above 0.05).

CONCLUSIONSHst1 can promote the proliferation and migration of HaCaT cells. It has synergic effect with rhEGF on the promotion of cell proliferation, but their synergic effect on cell migration is not obvious.

Cell Cycle ; drug effects ; Cell Line ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Epidermis ; cytology ; Histatins ; pharmacology ; Humans ; Wound Healing