No abstract available.
Cell Cycle*

No abstract available.
Cell Cycle*

No abstract available.
Cell Cycle* ; Endothelial Cells*

PURPOSE: The study was aimed to detect the induction of apoptosis, cell cycle arrest and calcified nodule formation after irradiation on primarily cultured osteoblasts. MATERIALS AND METHODS: Using rat calvarial osteoblasts, the effects of irradiation on apoptosis, cell cycle arrest, and calcified nodule formation were studied. The single irradiation of 10, 20 Gy was done with 5.38 Gy/min dose rate using the 137Cs cell irradiator at 4th and 14th day of culture. Apoptosis induction and cell cycle arrest were assayed by the flowcytometry at 1, 2, 3, and 4 days after irradiation. The formation of calcified nodules was observed by alizarin red staining at 1, 3, 10, 14 days after irradiation at 4th day of culture, and at 1, 4, 5 days after irradiation at 14th day of culture. RESULTS: Apoptosis was not induced by 10 or 20 Gy independent of irradiation and culture period. Irradiation did not induced G1 arrest in post-irradiated ostedblasts. After irradiation at 4th-day of culture, G2 arrest was induced but it was not statistically significant after irradiation at 14th-day of culture. In the case of irradiated cells at 4th day of culture, calcified nodules were not formed and at 14th-day of culture after irradiation, calcified nodule formation did not affected. CONCLUSION: Taken together, these results suggest that irradiation at the dose of 10-20 Gy would not affect apoptosis induction of osteoblasts. Cell cycle and calcified nodule formation were influenced by the level of differentiation of osteblasts.
Animals ; Apoptosis* ; Cell Cycle Checkpoints* ; Cell Cycle* ; Osteoblasts* ; Rats*

OBJECTIVE: The effectiveness of gamma knife radiosurgery to malignant glioma has been controversial. The goal of this study is to elucidate the in vitro biological response of malignant glioma cells to gamma knife radiosurgery. METHODS: The human glioma cell lines U87 MG (p53-wild type) and U373 MG (p53-mutant type) were irradiated in vitro via Gamma Knife 23004B2 using specially designed well holder, with a maximal dose of 10, 20, 40, 80Gy. Those two cell lines were used to study a variety of gamma knife effects on morphological change by microscopic observation, on cell viability by MTT assay, on postirradiated apoptosis by annexin assay, and on cell cycle by flow cytometry. RESULTS: With increasing dosage, more spheroid cells were observed in tumor cells and this phenomenon peaked at the second day after gamma knife irradiation. MTT assay performed 3 hours after irradiation revealed reduced cell survival in the cells irradiated with over 20Gy (p=0.000). The annexin assay showed that apoptosis tended to increase on escalating the radiation dose in U87 cells. G2-M phase cell cycle arrest markedly increased 48 hours after irradiation, and this was more exaggerated in U373 MG than in U87 MG. CONCLUSION: These results suggest that the biological effect of gamma knife on malignant glioma cell line in vitro is mainly mediated by G2-M phase cell cycle arrest.
Apoptosis ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Cell Survival ; Flow Cytometry ; Glioma* ; Humans ; Radiosurgery

PURPOSE: Phenylbutyrate is an effective redifferentiating agent in several human cancers. Recently phenylbutyrate has been reported to inhibit histone deacetylase activity. We investigated the effects of sodium 4-henylbutyrate (Na-4-PB) on cell proliferation in a human pancreatic cancer cell line. METHODS: A human pancreatic cancer cell line, Aspc-1 was purchased from Korean Cell Line Bank. Antiproliferative effects of sodium 4-phenylbutyrate were measured by MTT assay and their mechanisms were evaluated by apoptosis assay and cell cycle analysis. RESULTS: After 3 days of treatment with Na-4-PB at the concentration of 2.5, 5, 7.5, and 10 mM, relative growth inhibition compared to control was 21.3+/-8.3% (mean+/-SD), 37.8+/-2.3%, 46.7+/-0.5%, and 56.7+/-1.7% respectively (p < 0.05). Antiproliferative effect of Na-4-PB was also time-dependent. Combination treatment with Na-4-PB and troglitazone, a PPARg agonist, increased antiproliferative effects but was not synergistic. After 48 hour treatment with Na-4-PB, early apoptotic cell population in control, 2.5, and 5 mM of Na-4-PB was 29.6%, 44.2%, and 65.9%, respectively. After 24 hour treatment with Na-4- PB, G0/G1 phase population in control, 2.5, and 5 mM of Na-4-PB was 55.0%, 67.4%, and 65.8%, respectively. CONCLUSION: Na-4-PB inhibited pancreatic cancer cell proliferation by inducing apoptosis and cell cycle arrest at G0/G1 phase in time- and dose-dependent manner. Combination treatment with Na-4-PB and other chemotherapeutic agents such as troglitazone, a PPARg agonist, can enhance antiproliferative effects. Na-4-PB might be a promising potential therapeutic agent for patients with pancreatic cancer.
Apoptosis ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Cell Proliferation ; Histone Deacetylases ; Humans ; Pancreatic Neoplasms* ; Sodium

No abstract available.
Cell Cycle* ; Humans* ; Periodontal Ligament* ; Stress, Mechanical*

Cell Cycle Proteins ; Microtubule-Associated Proteins

Polyploid cells, which contain more than one set of chromosome pairs, are very common in nature. Polyploidy can provide cells with several potential benefits over their diploid counterparts, including an increase in cell size, contributing to organ growth and tissue homeostasis, and improving cellular robustness via increased tolerance to genomic stress and apoptotic signals. Here, we focus on why polyploidy in the cell occurs and which stress responses and molecular signals trigger cells to become polyploid. Moreover, we discuss its crucial roles in cell growth and tissue regeneration in the heart, liver, and other tissues.
Humans ; Liver ; Hepatocytes ; Cell Cycle ; Polyploidy ; Homeostasis

PURPOSE: Retinonic acid (RA) has been reported to induce differentiation and growth inhibition in various head and neck squamous cancer cell (HNSCC) lines. We hypothesized that this growth inhi bition might be explained by RA-induced apoptosis on cell cycle arrest mechanism. Therefore, we studied the degree of RA-induced apoptosis with variable RA concentration and exposure duration. MATERIAL AND METHODS: The flow cytometric evaluation of apoptosis degree and cell cycles were carried out with 7-amino actinomycin D (7AAD) and propium iodide (PI) respectively, with var ious RA exposure durations (2, 3, 6 day) and concentrations (conrol, 10 6, 10 7, 10 8, 10 9, 10 10 mole). Two different HNSCC lines (1483, SqCC/Y1) were used and the experiment was repeated twice. RESULTS: The maximal fraction of apoptosis in 1483 and SqCC/Y1 cell lines were observed at same concentration and exposure duration (1483: 6th day & 10 6, mole, and SqCC/Y1: 6th day & 10 6 mole). In our experimental model, RA did not induce specific cell cycle arrest in these HNSCC lines. However we observed S phase fraction increase in SqCC/Y1 cell line after RA treatment. CONCLUSION: We suppossed that in HNSCC lines, RA-induced cell growth inhibition could be explained by not only RA-induced apoptosis but also cell cycle arrest. Futher, in vitro study has been carried out to elucidate the RA-iduced cell growth inhibition mechanism in our laboratory.
Apoptosis ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Dactinomycin ; Head* ; Models, Theoretical ; Neck* ; S Phase ; Tretinoin