OBJECTIVETo assess the effects of tumor necrosis factor-α (TNF-α) in enhancing the radiosensitivity of lung cancer cells in vitro.

METHODSA549 cells were exposed to γ-ray with or without TNF-α treatment. MTT assay was used to evaluate the cell viability, and flow cytometry was performed to assess the cell apoptosis. Western blotting was used to observe the expression of caspase-3 protein in the exposed cells.

RESULTSCompared with the exposed cells without TNF-α treatment, the cells treated with TNF-α showed significantly suppressed cell proliferation, increased the cell apoptosis, altered cell cycle, and increased caspase-3 protein expression after γ-ray exposure.

CONCLUSIONTNF-α can enhance the radiosensitivity of A549 cells to increase the efficiency of radiotherapy with γ-ray irradiation.

Apoptosis ; drug effects ; radiation effects ; Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Gamma Rays ; Humans ; Lung Neoplasms ; Radiation Tolerance ; drug effects ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo investigate the effect of curcumin (Cur) on radiosensitivity of nasopharyngeal carcinoma cell CNE-2 and its mechanism.

METHODThe effect of curcumin on radiosensitivity was determined by the clone formation assay. The cell survival curve was fitted by Graph prism 6. 0. The changes in cell cycle were analyzed by flow cytometry (FCM). The differential expression of long non-coding RNA was detected by gene chip technology. Part of differentially expressed genes was verified by Real-time PCR.

RESULTAfter 10 micro mol L-1 Cur had worked for 24 h, its sensitization enhancement ratio was 1. 03, indicating that low concentration of curcumin could increase the radiosensitivity of nasopharyngeal carcinoma cells; FCM displayed a significant increase of G2 phase cells and significant decrease of S phase cells in the Cur combined radiation group. In the Cur group, the GUCY2GP, H2BFXP, LINC00623 IncRNA were significantly up-regulated and ZRANB2-AS2 LOC100506835, FLJ36000 IncRNA were significantly down-regulated.

CONCLUSIONCur has radiosensitizing effect on human nasopharyngeal carcinoma CNE-2 cells. Its mechanism may be related to the changes in the cell cycle distribution and the expression of long non-coding IncRNA.

Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Curcumin ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; radiation effects ; Humans ; RNA, Long Noncoding ; genetics ; Radiation Tolerance ; drug effects

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

AIMTo study effect of soybean isoflavones (SI) on spleen in radiated mice.

METHODS90 male mice were randomly divided into control group, radiated group, radiated plus 0.5% dose SI group. After 2-week feeding, the mice received 4.0 Gy 137Cs gamma-radiation, the cell cycles, cell apoptosis and proliferation on the spleen and the spleen index were observed in radiated after 12 h, 24 h, 1 week and 2 weeks.

RESULTSAfter the mice were radiated, the spleen were significantly atrophy, the rate of the cell apoptosis and the cell cycles of G0-G1 phase in splenocytes were significantly increased (P < 0.01), the cell cycles rate of S phase and the proliferation index were significantly decreased in spleen (P < 0.05). Compared with radiated group, the spleen atrophy and the rate of the cell cycles of G0-G1 phase were significantly decreased (P < 0.05), and the cell cycles of G2-M phase and the proliferation index were significantly increased (P < 0.05) in the mice supplied 0.5% soybean isoflavones.

CONCLUSIONThe soybean isoflavones could significantly increase spleen radioprotective effect in mice.

Animals ; Apoptosis ; drug effects ; radiation effects ; Cell Cycle ; drug effects ; radiation effects ; Cellular Structures ; Isoflavones ; pharmacology ; Male ; Mice ; Mice, Inbred Strains ; Radiation, Ionizing ; Soybeans ; Spleen ; cytology

OBJECTIVETo study the radiosensitizing effect of gefitinib on nasopharyngeal carcinoma cell line CNE2 in vitro.

METHODSNasopharyngeal carcinoma cell line CNE2 was cultured in RP2MI 1640. MTT assay was performed to evaluate the cell proliferation changes in response to gefitinib treatment and the radiosensitizing effect of gefitinib. The cell survival curves and sensitive enhancement ratio (SERs) were obtained with a clonogenic assay. Flow cytometry analysis was applied to detect the cell cycle changes and cell apoptosis.

RESULTSMTT assay showed that cells exposed to gefitinib and radiation had a significantly lower survival ratio compared to the cells with radiation exposure only (0.582∓0.012 vs 0.398∓0.016, P=0.002), with a SER of 1.535∓0.134. The S phase cell percentage was significantly decreased and G(2)-M phase cells increased in gefitinib plus radiation group (P=0.000), suggesting a synergistic effect of gefitinib and radiation.

CONCLUSIONGefitinib can enhance the radiosensitivity of nasopharyngeal carcinoma CNE2 cells in vitro possibly by inhibiting cell proliferation, inducing cell apoptosis, and causing changes in the cell cycle distribution.

Apoptosis ; drug effects ; Carcinoma ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Flow Cytometry ; Humans ; Nasopharyngeal Neoplasms ; pathology ; Quinazolines ; pharmacology ; Radiation Tolerance ; drug effects

OBJECTIVETo evaluate the effect of gemcitabine in enhancing the radiosensitivity of hepatoma cell line HepG2 and explore its mechanisms.

METHODSClonogenic survival assay is employed to calculate the ratios of L-Q model radiation biology parameters and radiosensitization after different doses of irradiation. Flow cytometry was used to detect the changes in HepG2 cell cycle and apoptosis rate after gemcitabine treatment and radiation exposure.

RESULTSThe survival fraction at 2 Gy of HepG2 cells treated with gemcitabine was significantly lower, and the value of alpha was significantly higher than those of untreated cells. GEM treatment increased the percentage of radiation-induced G0/G1 phase cells and cell apoptosis.

CONCLUSIONGemcitabine can significantly enhance the radiosensitivity of HepG2 cells by enhancing radiation-induced cell cycle arrest in G0/G1 phase and cell apoptosis.

Apoptosis ; drug effects ; Cell Cycle Checkpoints ; drug effects ; Deoxycytidine ; analogs & derivatives ; pharmacology ; Hep G2 Cells ; Humans ; Radiation Tolerance ; drug effects ; Radiation-Sensitizing Agents ; pharmacology

OBJECTIVETo explore the radiosensitizing effect of erlotinib on human lung adenocarcinoma cell line A549 cells and the related mechanisms.

METHODSThe inhibitory effect of erlotinib on A549 cells was assessed by MTT assay, and its IC50 concentration was calculated. The radiosensitization was evaluated by the method of clone forming assay. Flow cytometry was used to analyze the effect of erlotinib on cell cycle and apoptosis.

RESULTSThe growth of A549 cells was inhibited after the cells were exposed to erlotinib for 48 hours. Moreover, the inhibitory rates increased with the increase of erlotinib concentrations, and IC50 was 19.26 µmol/L. In contrast to the irradiation alone group, the survival rates of the cells in erlotinib plus irradiation groups decreased, and erlotinib enhanced the radiosensitivity of the A549 cells. This effect was further increased as cells were exposed to erlotinib for a longer time. In the irradiation alone group and the two groups exposed to erlotinib for 24 hours and 48 hours before irradiation, D0 values were 3.01 Gy, 2.58 Gy and 2.45 Gy respectively, and Dq values were 2.16 Gy, 1.94 Gy and 1.61 Gy, respectively. In the last two groups, SERD0 values were 1.17 and 1.23, respectively. The flow cytometry analysis showed that erlotinib induced G2/M phase arrest and increased the apoptosis rate in A549 cells. With the increase of exposure time, the effects were more significant.

CONCLUSIONSErlotinib inhibits the A549 cell growth and enhances the radiosensitivity of A549 cells in vitro. The radiosensitizing mechanisms might be related to inhibiting repair of sublethal injury and inducing G2/M phase arrest and apoptosis.

Adenocarcinoma ; pathology ; Apoptosis ; drug effects ; radiation effects ; Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; radiation effects ; Dose-Response Relationship, Drug ; Erlotinib Hydrochloride ; Humans ; Lung Neoplasms ; pathology ; Particle Accelerators ; Quinazolines ; administration & dosage ; pharmacology ; Radiation Tolerance ; drug effects ; Radiation-Sensitizing Agents ; administration & dosage ; pharmacology

OBJECTIVETo examine UVB-induced responses in normal human keratinocytes (HaCaT) and epidermoid carcinoma cells (A431) at the cellular and molecular level, and investigated the protective effect of salidroside.

METHODSCells irradiated by UVB at various dosage and their viability was assessed by MTT assays, cell cycle was analysed by flow cytometry. The expression of NF-κB, BCL-2, and CDK6 after 50 J/m(2) UVB irradiation were detected by RT-PCR and western blotting.

RESULTSOur results confirmed greater tolerance of A341 cells to UVB-induced damage such as cell viability and cell cycle arrest, which was accompanied by differential expression changes in NF-κB, BCL-2, and CDK6. UVB exposure resulted in HaCaT cells undergoing G(1)-S phase arrest. When treated with salidroside, HaCaT survival was significantly enhanced following exposure to UVB, suggesting great therapeutic potential for this compound.

CONCLUSIONTaken together, our study suggests that A431 respond differently to UVB than normal HaCaT cells, and supports a role for NF-κB, CDK6, and BCL-2 in UVB-induced cell G(1)-S phase arrest. Furthermore, salidroside can effectively protect HaCaT from UVB irradiation.

Antioxidants ; pharmacology ; Apoptosis ; radiation effects ; Carcinoma, Squamous Cell ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Gene Expression Regulation, Neoplastic ; Glucosides ; pharmacology ; Humans ; Keratinocytes ; radiation effects ; Phenols ; pharmacology ; Ultraviolet Rays

OBJECTIVEThe effect of angelica sinensis polysaccharides (ASP) on the production of reactive oxygen specie (ROS), the capability of total anti-oxidant (T-AOC), and the expression of p16 in mRNA level in mice hematopoietic stem cells (HSCs) were observed to explore the underlying mechanism that ASP delay aging of HSCs in vivo.

METHODC57BL/6J mice were randomly divided into normal group, aging group, and the above groups treated with ASP. Mice were uniformly explored in X-ray (3.0 Gy/8 F) to erect model of aging. Normal and aging ASP intervention groups mice were treated with ASP by intragastric administration, while normal and aging groups were treated with equal-volume NS during X-ray irradiation. Mice HSCs were isolated by magnetic cell sorting and cultured in vitro. Senescence-associated beta-galactosidase (SA-beta-Gal) staining was used to detect aging HSCs. Cell cycles analysis and CFU-Mix cultivation were used to evaluate the capability of self-renewing and colony forming in HSCs. The production of ROS in HSCs was evaluated by flow cytometry analysis and immunofluorescence assess, respectively. T-AOC was detected by chemical colorimetric method. The expression of p16 was determined by real-time quantitative PCR (qRT-PCR).

RESULTExogenous X-ray irradiation induced HSCs aging was compared with normal group without irradiation. Biological feature of HSCs in aging group with X-ray irradiation as follows: The percentage of SA-beta-Gal positive cells, the ratio of G1 stages and the production of ROS were significantly increased , the expression of p16 in mRNA level was also upregulated. The capacility of colony forming and T-AOC in HSCs were decreased. ASP could significantly decrease the percentage of SA-beta-Gal positive cells, the ratio of G1 stages and the production of ROS in HSCs, and downregulate the expression of p16 in mRNA level in HSCs contrast to aging group without ASP treatment. In addition, ASP could remarkably increase T-AOC and the capacility of colony forming in HSCs compared with aging group without ASP treatment.

CONCLUSIONX-ray (3.0 Gy/8 F) could induce mice HSCs aging. ASP could delay senescence HSCs aging which maybe partly ascribed to the inhibition of oxidative damage and the downregulation of p16 mRNA expression.

Aging ; drug effects ; radiation effects ; Angelica sinensis ; chemistry ; Animals ; Cell Cycle ; drug effects ; radiation effects ; Cells, Cultured ; Cellular Senescence ; drug effects ; radiation effects ; Cyclin-Dependent Kinase Inhibitor p16 ; genetics ; Female ; Flow Cytometry ; Gene Expression ; drug effects ; radiation effects ; Hematopoietic Stem Cells ; drug effects ; metabolism ; radiation effects ; Male ; Mice ; Mice, Inbred C57BL ; Oxidative Stress ; drug effects ; radiation effects ; Polysaccharides ; pharmacology ; Random Allocation ; Reactive Oxygen Species ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; X-Rays ; beta-Galactosidase ; metabolism

OBJECTIVETo evaluate the radiosensitization of paclitaxel combined with radiation on nasopharygneal carcinoma cells( CNE-I) in vitro.

METHODSHuman CNE-I cells were used for this study. Clonogenic assay was used to determine the drug dose of IC10, IC50 and IC90 for CNE-I Cells. The cells treated with different concentration of paclitaxel for 24 hours before or after radiation (dose ranged from 0 - 10 Gy ) were used to evaluate the radiosensitizing effect of paclitaxel combined with radiation. DNA flow cytometry was performed to define the cell cycle characteristics of cell populations treated for 0, 2, 6, 12, 18, 24 h with 0.1 nmol/L, 0.5 nmol/L, 1.0 nmol/L, 2.5 nmol/L paclitaxel, respectively.

RESULTSThe dose of IC10, IC50 and IC90 for paclitaxel in CNE-I cells was 0.05 nmol/L, 1.0 nmol/L and 2.5 nmol/L, respectively. Paclitaxel treatment at concentration of 0.05 nmol/L and 1.0 nmol/L for 24 hours combined with X-ray irradiation before or after radiation showed radiosensitivity-enhansing effects in CNE-I cells. G2/M block was present when the drug concentrations were 2.5 nmol/L and 10.0 nmol/L, and it peaked at 18 hours.

CONCLUSIONWith an optimal paclitaxel/radiation combination, paclitaxel may exert a radiosensitizing effect on CNE-I cells. The effect might be related to the G2/M block caused by paclitaxel.

Antineoplastic Agents, Phytogenic ; pharmacology ; Carcinoma, Squamous Cell ; pathology ; Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Humans ; Nasopharyngeal Neoplasms ; pathology ; Paclitaxel ; administration & dosage ; pharmacology ; Particle Accelerators ; Radiation Tolerance ; drug effects ; Radiation-Sensitizing Agents ; pharmacology