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 seek for the appropriate concentration, at which IGF-II can exerts its strong effects on postirradiation proliferation, physiological function and differentiation of the rat's osteoblast-like cells (ROB).

METHODSThe osteoblast-like cells used were isolated from the calvariae of neonatal (one-day-old) SD rats by sequential enzymatic digestion. The third passages of the cells were irradiated with gamma-ray from a (60)Co source at the doses of 100, 400, 600, and 900 cGy. The medium was changed immediately after irradiation and 5 concentrations of IGF-II, i.e., 0, 0.1, 1.0, 10.0, and 100.0 microgram/L were added. 6 days after radiation (9 days in culture), the examination, or the measurement of relative cell number, was carried out.

RESULTSRadiation inhibited the ROB, even lethally. IGF-II completely counteracted the inhibitory effects when the cells were exposed to the radiation at lower dose (100 cGy), and partially when at higher dose (400 cGy). But after the radiation at much higher dose as 900 cGy, the damages were irreversible, even with the existence of this growth factor.

CONCLUSIONSAt least a portion of effective recovery of postirradiation damages may be due to IGF-II-induced radioresistance. Incubation with IGF-II can increase radioresistance or repair of radiation-induced cells damages. However, this effect depends on the dose of radiation.

Animals ; Cell Division ; drug effects ; radiation effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Insulin-Like Growth Factor II ; pharmacology ; Osteoblasts ; drug effects ; physiology ; radiation effects ; Radiation Tolerance ; drug effects ; Rats ; Rats, Sprague-Dawley

Inevitable human exposure to ionizing radiation from man-made sources has been increased with the proceeding of human civilization and consequently public concerns focus on the possible risk to human health. Moreover, Fukushima nuclear power plant accidents after the 2011 East-Japan earthquake and tsunami has brought the great fear and anxiety for the exposure of radiation at low levels, even much lower levels similar to natural background. Health effects of low dose radiation less than 100 mSv have been debated whether they are beneficial or detrimental because sample sizes were not large enough to allow epidemiological detection of excess effects and there was lack of consistency among the available experimental data. We have reviewed an extensive literature on the low dose radiation effects in both radiation biology and epidemiology, and highlighted some of the controversies therein. This article could provide a reasonable view of utilizing radiation for human life and responding to the public questions about radiation risk. In addition, it suggests the necessity of integrated studies of radiobiology and epidemiology at the national level in order to collect more systematic and profound information about health effects of low dose radiation.
DNA Damage/drug effects ; Environmental Exposure ; Humans ; Leukemia/epidemiology/etiology ; Neoplasms, Radiation-Induced/epidemiology ; *Radiation Dosage ; Radiation Tolerance ; *Radiation, Ionizing ; Radioactive Hazard Release ; Risk

Radiotherapy, frequently used for treatment of solid tumors, carries two main obstacles including acquired radioresistance in cancer cells during radiotherapy and normal tissue injury. Phenylpropanoids, which are naturally occurring phytochemicals found in plants, have been identified as potential radiotherapeutic agents due to their anti-cancer activity and relatively safe levels of cytotoxicity. Various studies have proposed that these compounds could not only sensitize cancer cells to radiation resulting in inhibition of growth and cell death but also protect normal cells against radiation-induced damage. This review is intended to provide an overview of recent investigations on the usage of phenylpropanoids in combination with radiotherapy in cancer treatment.
Antineoplastic Agents/*therapeutic use ; Apoptosis/drug effects/radiation effects ; Chromones/therapeutic use ; Combined Modality Therapy ; Cytoprotection/drug effects/radiation effects ; Humans ; Neoplasms/pathology/*radiotherapy ; Phenylpropionates/therapeutic use ; Plants ; Radiation Tolerance/drug effects ; Radiation-Sensitizing Agents/*therapeutic use ; *Radiotherapy

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 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

OBJECTIVETo investigate the effects of the ultra-filtration extract mixture from Hedysarum Polybotrys (UEMHP) on the radiosensitivity of HepG2 cells, and to explore its possible mechanisms.

METHODSThe proliferation inhibition effects of UEMHP on HepG2 cells was detected by CCK-8 assay. The colony formation assay was used for the survival fraction (SF) analysis. The distribution of the cell cycle and the apoptosis rate were detected using flow cytometry (FCM). The survivin mRNA expression level was detected using reverse transcription-PCR assay.

RESULTSThe inhibition of UEMHP on HepG2 cells was time-and dose-dependent at the concentration ranging between 5 -50 mg/L (P < 0.05). The parameters of the two curve for SF (P < 0.05) showed statistical difference between the irradiation group and the UEMHP irradiation group. UEMHP could inhibit the clone formation of HepG2 cells and enhance the radiosensitivity of HepG2 cells. The results of FCM showed that UEMHP could induce G2/M phase arrest. The apoptosis rate in the UEMHP irradiation group (21.42% +/- 3.74%) was higher than that in the control group (5.35% +/- 0.41%), the only UEMHP group (10.36% +/- 1.75%), or the irradiation group (10.58% +/- 2.01%) (P < 0.01). RT-PCR showed that the survivin mRNA expression level was lower in the UEMHP irradiation group (0.31 +/- 0.02) than in the control group (0.82 +/- 0.06) and the irradiation group (0.58 +/- 0.04) respectively, showing statistical difference (P < 0.01).

CONCLUSIONUEMHP can enhance the radiosensitivity of HepG2 cells, and its possible mechanisms might be correlated to down-regulating the survivin mRNA expression and promoting the apoptosis.

Apoptosis ; Cell Proliferation ; drug effects ; radiation effects ; Drugs, Chinese Herbal ; pharmacology ; Hep G2 Cells ; Humans ; Inhibitor of Apoptosis Proteins ; metabolism ; Radiation Tolerance ; drug effects

Drug Resistance, Neoplasm ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Female ; Humans ; Ovarian Neoplasms ; drug therapy ; radiotherapy ; Radiation Tolerance

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