No abstract available.
Animal ; Apoptosis/*drug effects ; Human ; Tumor Cells, Cultured

Apoptosis ; drug effects ; Cell Division ; drug effects ; Esophageal Neoplasms ; pathology ; Humans ; Selenomethionine ; pharmacology ; Tumor Cells, Cultured

This study was purposed to investigate the biological effect of vinblastine (VLS), usually known as inductor of mitotic arrest, on MOLT-4 of ALL cells and to evaluate its significance. The cell arrest in M phase and/or cell apoptosis were induced by treatment of MOLT-4 cells with 0.05 microg/ml VLS for 0 - 12 hours; the DNA histogram was detected by flow cytometry; the morphological changes of cells were observed by confocal microscopy; the cell cycle distribution, cell apoptosis and morphological changes of cells before and after arrest were analyzed by using arrest increasing rate (AIR), arrest efficiency (AE), apoptosis rate (AR) and morphologic parameters respectively. The results indicated that the cell arrest did not accompanied by significant increase of apoptosis rate; the DNA histogram of cell arrest showed dynamic change of cell cycle in time-dependent manner; the arrest efficiency could be quantified. The cell arrest at M phase was accompanied by cell stack in S phase, the cell proliferation rate dropped after cell arrest occurred. The cells arrested at M phase possessed of characteristic morphologic features in cell mitosis. It is concluded that the vinblastine can solely induce arrest of MOLT-4 cells at M phase. This study provides experimental basis for further investigating the relation of cell cycle arrest to apoptosis, mechanism of checkpoint and development of new anticancer drugs.
Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Flow Cytometry ; Humans ; Tumor Cells, Cultured ; Vinblastine ; pharmacology

OBJECTIVETo study the effect of acrylonitrile (ACN) to cell growth, apoptosis, proliferation and related gene expression of rat normal glial cells (DI TNC1) and tumor glial cells (C6).

METHODSThe concentration of ACN on DI TNC1 and C6 were 25, 50 and 75 microg/ml. For cell growth, proliferation and apoptosis assay, the treated time was 24 hours, for microarray assay, the treated time was 4 and 24 hours.

RESULTSAfter treatment of DI TNC1 cell with 25,50 and 75 microg/ml ACN, the DNA synthesis index were decreased 93.1%, 81.3% and 74.9% as compared to control respectively, the apoptosis index was increased 118%, 122% and 143% as compared to controls respectively. The DNA synthesis and apoptosis indexes of C6 cell showed no change after treatment with ACN. The cell cycle and apoptosis pathway related genes, such as cyclin and p53, also showed changes after treatment with ACN.

CONCLUSIONACN inhibited the cell proliferation of DI TNC1, induced the apoptosis of DI TNC1 and had no effect on cell proliferation and apoptosis of C6 cells, and the related regulation gene expression changes further confirmed the results.

Acrylonitrile ; toxicity ; Air Pollutants ; toxicity ; Animals ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Gene Expression ; Neuroglia ; cytology ; drug effects ; Rats ; Tumor Cells, Cultured

A new photosensitizer, CpD(chlorophyll derivatives), previously reported as a promising agent for tumor therapy, was studied to determine its inhibitory effects on Gross leukemia virus(GLV), a mouse retrovirus isolated from the GLV-producing TGV cell line, and the cytocidal effect on the GLV infected cells in vitro, following photodynamic treatment with CpD-D and red light, the viral inactivation and infectivity were examined by measuring the reverse transcriptase(RT) activity of the virus itself and that in cell-free culture supernatant of freshly GLV-infected secondary mouse embryo cells respectively. The cytocidal activity was measured by trypan blue exclusion test. Inhibition of GLV associated RT activity resulted from CpD-D and red light treatment. The RT inhibition effect was immediate and the infectivity of these photodynamically treated GLV to mouse embryo cells was also inhibited. However, specific cytotoxicity of GLV infected cells was not found. Thus, it is concluded that CpD-D may be used as an effective antiviral agent.
Animal ; Chlorophyll/*pharmacology ; Gross Virus/*drug effects ; Leukemia, Experimental/*drug therapy ; Mice ; *Photochemotherapy ; Tumor Cells, Cultured

The study was aimed to explore the stimulatory effect of tumor necrosis factorα (TNF-α) on differentiation and maturation of human peripheral blood mononuclear cell-derived dendritic cells (PBMNCDC). 30 ml of peripheral blood from healthy volunteers were collected, the PBMNC were isolated according to Thomas' method and were cultured with incubation of granulocyte/macrophage colony stimulating factor (GM-CSF), interleukin-4 (IL-4) for 8 day, and TNF-α was added on day 5. The expression of HLA-DR, CD83 and CD1a on surface of DC were detected by flow cytometry, the ability of DC to stimulate the proliferation of allogenic T cells was evaluated by MTT assay. The results showed that the TNF-α could up-regulate the expression of HLA-DR, CD83 and CD1a and activated DC could enhance the proliferation of allogenic T cells. Furthermore, the TNF-α at the concentration of 20 ng/ml was more effective. It is concluded that the TNF-α can effectively enhance the functional differentiation and maturation of the PBMNCDC and TNF-α at the concentration of 20 ng/ml is most effective to enhance differentiation and maturation of DC.
Cell Differentiation ; drug effects ; Cells, Cultured ; Dendritic Cells ; cytology ; drug effects ; Flow Cytometry ; Humans ; Tumor Necrosis Factor-alpha ; pharmacology

Experimental data suggest that Resveratrol, a compound found in grapes and other fruits may influence cell proliferation and apoptosis. The aim of our experiments was to study the effect of Resveratrol on tumor cell cultures and an endothelial cell culture in order to examine the effect of various doses of this compound on active cell death and cell proliferation. Human tumor (HT-29, SW-620, HT-1080) and endothelial (HUV-EC-C) cells were treated with various doses of (0.1 to 100.0 microg/ml) Resveratrol in vitro. Cell number, apoptotic and mitotic index was measured 24, 48 and 72 h after treatment. Low doses (0.1-1.0 microg/ml) of Resveratrol enhance cell proliferation, higher doses (10.0-100.0 microg/ml) induce apoptosis and decrease mitotic activity, which is reflected in changes of cell number. Resveratrol influences dose dependently the proliferative and apoptotic activity of human tumor and endothelial cells. The possible role of formaldehyde in the mechanism of action of Resveratrol is discussed.
Antineoplastic Agents, Phytogenic/pharmacology* ; Apoptosis* ; Cells, Cultured ; Dose-Response Relationship, Drug ; Endothelium/drug effects* ; Endothelium/cytology ; Human ; Mitosis/drug effects* ; Stilbenes/pharmacology* ; Tumor Cells, Cultured

Flavone compound is a polyphenolic compound widely existing in plants and has an extensive biological activity. In recent years, it has been found to have a significant anti-cancer effect, as in combating cell proliferation, inducing cell apoptosis, interfering with cellular signal transduction, increasing the activity of the cancer repressor gene and inhibiting the expression of oncogene. This paper reviews the mechanism by which flavone compound, induces the apoptosis of prostate cancer cells.
Animals ; Apoptosis ; drug effects ; Flavones ; pharmacology ; Humans ; Male ; Prostatic Neoplasms ; pathology ; Rats ; Tumor Cells, Cultured

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; pathology ; Glucosamine ; pharmacology ; Humans ; Liver Neoplasms ; pathology ; Tumor Cells, Cultured

OBJECTIVETo investigate the effects of progesterone on the growth and migration of breast cancer cells.

METHODSMCF-7 and T-47D cells were cultured in DMEM and stimulated with 100 nmol/L progesterone for 48 h, and the cell proliferation was evaluated by MTT assay, cell migration by wound-healing assay and E-catherin expression by Western blotting.

RESULTSProgesterone stimulated the cell proliferation and migration and down-regulated the expression of E-catherin in both MCF-7 and T-47D cells.

CONCLUSIONSProgesterone stimulates the cell proliferation and migration of cultured breast cancer cells, suggesting the clinical significance of anti-progesterone therapy in breast cancer.

Breast Neoplasms ; pathology ; Cadherins ; metabolism ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Female ; Humans ; Progesterone ; pharmacology ; Tumor Cells, Cultured