OBJECTIVETo evaluate the effects of Bisnaphthalimide (C8) on the proliferation and apoptosis of SMMC-7721 cells.

METHODSThe effects of C8 on the proliferation of SMMC-7721 cells were evaluated by MTT. Cell cycle and apoptotic cell percentage were studied by flow cytometry. The protein of Bcl-2 was detected by Western blot. The intra-cellular protein of Bcl-2 was detected by flow cytometry. The proteins of caspase9 and caspase3 were detected by ELISA.

RESULTSC8 inhibited the growth of SMMC-7721 cells. The IC50 of C8 on SMMC-7721 cells was 15 micromol/L. C8 initiated apoptosis of SMMC-7721 cells. After SMMC-7721 cells were exposed to C8 in concentrations of 10, 15, 20 micromol/L, the apoptosis rates were 16.8%, 29.4% and 35.8%, respectively, significantly higher than those of the controls (P less than 0.01). Flow cytometry and Western blot analysis showed that Bcl-2 protein level was inhibited after treatment with C8. The ELISA analysis showed that caspase9 and caspase3 were activated in the SMMC-7721 cells after the C8 treatment.

CONCLUSIONC8 could induce apoptosis of human liver cancer SMMC-7721 cells. C8 might be a potential efficient anticancer drug.

Apoptosis ; drug effects ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Naphthalimides ; pharmacology

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

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Genistein ; pharmacology ; Humans ; Nasopharyngeal Neoplasms ; pathology

OBJECTIVETo investigate the anti-tumor effects of melittin against malignant human glioma cells in vitro.

METHODSTwo malignant human glioma cell lines (U87 and U251) were treated with melittin at various concentrations, and the cell growth inhibition and apoptosis were evaluated using MTT assay, flow cytometry and agarose gel electrophoresis.

RESULTSMelittin could obviously inhibit the proliferation of the two glioma cell lines (P<0.05). At the concentrations of 1, 10, 20, 40, 80, 160, 200 mg/L, melittin resulted in U87 cell apoptosis rates of 12.80%, 16.92%, 22.69%, 34.05%, 41.82%, 59.87%, and 80.25%, and in U251 cell apoptosis rate of 11.61%, 16.21%, 22.03%, 30.57%, 41.10%, 58.33%, and 79.12%, respectively, showing a dose-dependent effect in its action of inducing cell apoptosis.

CONCLUSIONMelittin inhibits the proliferation and induces apoptosis of malignant human glioma cell lines in vitro.

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Glioma ; metabolism ; pathology ; Humans ; Melitten ; pharmacology

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Sulfinic Acids ; pharmacology

OBJECTIVETo investigate effects of two kinds of anti-cancer bioactive peptide (ACBP) on proliferation and cell cycle in human nasopharyngeal carcinoma strain CNE.

METHODSCell culture was used in vitro, CNE cells were exposed to different concentration ACBP, in all groups, contrast groups were set up. And 24, 48, 72 hours later, growth characteristics of CNE cells were studied by morphological observation and MTT assay . Cell cycle and apoptosis were analyzed by flow cytometry (FCM).

RESULTSIn normal contrast group, CNE cells grew intensively and contacted with each other. However, cells which were treated with ACBP were inhibitory greatly in higher dose ACBP group, necrosis could be found. MTT assay showed that ACBP inhibited growth of CNE cell. FCM showed that ACBP (20.0 microg/ml) could raise cell ratio of S phase and induce apoptosis of CNE cells. CNE cells were treated by two kind of ACBP (5.0 microg/ml) for 24 h, FCM showed that early apoptosis rate were (11.8 +/- 0.3)% and (8.1 +/- 0.2)% respectively, which showed statistical significance in comparison with control group (t = 42.535, 47.300 respectively, P = 0.000). Under light microscope, some sings of cell apoptosis including coagulation of chromatin, fragmentation of nuclei and apoptotic body could be found.

CONCLUSIONSTwo kinds of ACBP inhibited human nasopharyngeal carcinoma strain CNE proliferation and arrested the cells to S phase, also induced the cells to apoptosis. Nasopharyngeal neoplasms;

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Nasopharyngeal Neoplasms ; pathology ; Peptides ; pharmacology

OBJECTIVETo explore the effects of 1,2-dichloroethane (1,2-DCE) on the cellular proliferation, cellular cycle and apoptosis of SW620 cells in vitro.

METHODSSW620 cells were exposed to 1,2-DCE at different concentrations for 0.5 and 1 h. MTT assay was used to detect the relative number and relative viability, the low cytometry (FCM) assay was utilized to measure the cell cycle and apoptosis.

RESULTSThe results of MTT assay showed that the cellular relative viability decreased with the 1,2-DCE's dose and exposure time. Compared with the DMSO group, the relative cellular viability of cells exposed to 1,2-DCE at the doses of 75, 100, 125, 150, 175, 200 µmol/L for 1 h decreased (P<0.05 or P<0.01). Compared with the groups exposed to 1,2-DCE for 0.5 h, the relative cellular viability of cells exposed to 175 µmol/L 1,2-DCE for 1 h decreased significantly (P<0.01). IC(50) of cellular proliferation in cells exposed to 1,2-DCE for 0.5 h was 89.41 µmol/L, and 95% confidence interval was 85.23 to 93.79 µmol/L. IC(50) of cellular proliferation in cells exposed to 1,2-DCE for 1 h was 87.68 µmol/L, and 95% confidence interval was 83.71 to 91.82 µmol/L. The results of FCM indicated that compared with the control group, the G(0)/G(1) phase in groups exposed to 1,2-DCE at the doses of 25, 50, 100, 150 and 200 µmol/L for 1 h decreased significantly (P<0.05 or P<0.01), the S phase in groups exposed to 1,2-DCE at the doses of 25, 50 and 100 µmol/L for 1 h reduced significantly (P<0.05 or P < 0.01), the G(2)/M phase in groups exposed to 1,2-DCE at the doses of 25, 50, 100, 150 and 200 µmol/L for 1 h increased significantly (P<0.05 or P<0.01). However, 1,2-DCE could not induce apoptosis of SW620 cells.

CONCLUSION1,2-DCE could inhibit the proliferation of SW620 cells, and arrest SW620 cells at G(2)/M phase, but could not induce the apoptosis of SW620 cells in vitro.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Ethylene Dichlorides ; toxicity ; Humans

G-rich oligonucleotides (GROs) belong to a novel class of phosphodiester oligonucleotides. They can form G-tetramer structure which contributes to cell cycle arrest and growth inhibitory effects by non-antisense pathway. This study was aimed to investigate the biological effects of GRO-26B on leukemia cell lines. Cell proliferation of different cell lines were detected by using MTT method and trypan blue incorporation assay. Alteration of cell cycle was analyzed by using flow cytometry. Apoptosis was detected by using Annexin V/PI kit. Western blot was used to detect the expression level of cyclins and CDKs. Morphological features of GRO-26B-treated cells was observed by light microscopy and transmission electron microscopy (TEM). The results showed that GRO-26B could inhibit the proliferation of AML cell lines, such as U937 and NB4 cells in a dose-dependent manner. GRO-26B induced the cell cycle to be arrested at S phase in time-dependent manner, which was associated with the alteration of cyclin A, cyclin B, CDC2 and CDK2. The morphology of cells treated by GRO-26B also showed a distinct change as compared to the untreated cells. It is concluded that GRO-26B can inhibit AML cell proliferation, which is partially associated to cell cycle arrest at S phase. The S phase arrest is related to cyclins/CDKs. The regulation mechanism of cell cycle and proliferation is complicated. All of the above-mentioned phenomena need to be studied in the future.
Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Leukemia ; pathology ; Oligonucleotides ; pharmacology

OBJECTIVETo evaluate and explore the effects of 20(S)-ginsenoside Rh2 and 20(R)-ginsenoside Rh2 on the cytotoxicity, proliferation and the apoptosis of human lung adenocarcinoma A549 cells, and to illustrate the structure-activity relationship and possible mechanisms of anti-tumor active ingredients of ginseng.

METHODA549 cells were treated with different concentration gradient of ginsenoside Rh2 (S and R structure) and incubated for different time. Cell proliferation and cytotoxicity studies were detected by methyl thiazolyl tetrazolium (MTT) colorimetric assay, cell cycle and apoptotic was analyzed by PI stains and combination of Annexin V/Prop idium iodide double staining with flow cytometric analysis. The influences of activation on Caspase-3 were also detected by the immunofluorescence staining with fluorescence microscope.

RESULTMTT test indicated that ginsenoside Rh2 had a strong cytotoxicity activity to A549 cells. Ginsenoside Rh2 could obviously inhibit the cell proliferation in human lung adenocarcinoma cell line A549 at the effective doses of 25 mg x L(-1) treated with 48 h. The inhibition ratio and the value of IC50 for48 h of 20(R)-Rh2 and 20(S)-Rh2 were respectively 28.5%, 33.6% and 33.4, 28.5 mg x L(-1). The inhibition of ginsenoside Rh2 to A549 showed structure relationship significantly, time-dependent and concentration-dependent. Flow cytometric analysis (FACS) with PI stains analysis results showed that the proportion of A549 cells in G1 phase increased, while the number of cells in S phase decreased significantly and those in G2 phase reduced slightly. This result indicated structure relationship significantly, especially in the 20(S) -ginsenoside Rh2 inhibited the proliferation of A549 cell dramatically and retarded A549 cell cycle at G0/G1 phase. The immunofluorescent of combination with Annexin VFITC/PI by flow cytometric suggested ginsenoside Rh2 can induce inchoate apoptsis rate and late apoptosis rate of A549 cell significantly. All the results showed structure relationship significantly, especially in the 20(S)-ginsenoside Rh2. The immunofluorescent with fluorescence microscope suggested the activity of Caspase-3 were enhanced after ginsenoside Rh2 treated.

CONCLUSION20 (R) and 20(S)-ginsenoside Rh2 had a significant inhibitory effect on the proliferation. Compared with 20(S)-ginsenoside Rh2, 20 (S)-ginsenoside Rh2 has been shown to have significant anticancer effects and to be capable of blocking cell proliferation and causing G1 phase arrest in human lung adenocarcinoma A549 cells. 20 (R) and 20(S)-ginsenoside Rh2 have been shown to have anticancer effects and to be capable of increasing inchoate apoptotic rate, reducing apoptotic rate significantly, enhancing the activity of Caspase-3 and inducing apoptosis in human lung adenocarcinoma A549 cells.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Ginsenosides ; pharmacology ; Humans ; Microscopy, Fluorescence

OBJECTIVETo study radiation-enhancing effects on human gastric cancer MKN28 cell line and underlying mechanisms of β-elemene.

METHODSInhibition of MKN28 cell proliferation at different concentrations of β-elemene was assessed using the methyl thiazolyl blue colorimetric method (MTT method), with calculation of IC50 value and choice of 20% of the IC50 as the experimental drug concentration. Irradiation group and β-elemene+irradiation group were established, and the cell survival fraction (SF) was calculated from flat panel colony forming analysis, and fitted by the 'multitarget click mathematical model'. Draw the survival curve and get the radiobiological parameters D0, Dq, SF2, N and SER. Flow cytometry (FCM) was used to detect changes in the cell cycle and cell apoptosis rates was detected by Annexin-V/PI assay.

RESULTSβ-elemene exerted inhibitory effects on proliferation of gastric cancer MKN28 cells, with an IC50 of 45.6 mg/L and we chose 8 mg/L as the experimental concentration. The cell survival fraction of MKN28 cells with irradiation decreased significantly after treated with β-elemene; D0, Dq decreased, SER = 1.3. After combined treatment of β-elemene+irradiation, the results of FCM showed that cells could be arrested in the G2/M phase and the cell apoptosis increased significantly.

CONCLUSIONSβ-elemene can enhance the radiosensitivity of gastric cancer MKN28 cell line. Mechanistically, β-elemene mainly influences the cell cycle distribution of MKN28 cells by inducing G2/M phase arrest, inhibits the repair of sublethal damage and induces cell apoptosis to enhance the killing effects of radioactive rays.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Humans ; Radiation Tolerance ; drug effects ; Sesquiterpenes ; pharmacology ; Stomach Neoplasms ; pathology