Radiation-induced G2 phase arrest may contribute to the radioresistance of breast cancer stem cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate radiation-induced cell cycle changes of human breast cancer stem cells enriched by suspension culture.</p><p><b>METHODS</b>The tumorigenicity of human breast cancer stem cell line MCF-7 cultured in serum-free media was confirmed in NOD/SCID mice, and the radiosensitivity of the cells was tested by clone formation assay following radiation exposure. Flow cytometry was performed to evaluate radiation-induced cell cycle changes, and the protein expression of pCDC25C (ser216) was measured by Western blotting.</p><p><b>RESULTS</b>After the exposure to 2 Gy radiation, the survived fraction of the cells in suspension culture and those in adherent culture was 0.856 ∓ 0.061 and 0.783 ∓ 0.097, respectively, and the cells in suspension culture showed an obviously greater capacity of tumorigenicity in NOD/SCID mice. The radiation exposure resulted in an obvious increase in the proportion of G2 phase cells from (22.03 ∓ 2.12)% to (45.83 ∓ 2.25)% and significantly increased the expression of pCDC25C (ser216).</p><p><b>CONCLUSION</b>Radiation- induced G2 phase arrest may contribute to the resistance of the breast cancer stem cells to radiotherapy.</p>

Effect of shRNAmir lentiviral vector-mediated COX-2 silencing on the radiosensitivity of nasopharyngeal carcinoma cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the effect of COX-2 silencing on the radiosensitivity of a nasopharyngeal carcinoma (NPC) cell line C666-1.</p><p><b>METHODS</b>Anti-COX-2 C666-1 cell line with COX-2 gene silencing mediated by shRNAmir lentiviral vector and the control cell line Anti-GL-2 C666-1 were exposed to various radiation doses. The clonogenic survival assay and curve fitting was used to calculate the radiobiological parameters and the sensitization enhancement ratio after the radiation. Cell cycle changes were assessed after the exposure by flow cytometric analysis. In a BALB/c nude mouse model, the growth curve of the xenografts was generated and the tumor growth inhibition rate was calculated.</p><p><b>RESULTS</b>Compared with the control cells, Anti-COX-2 C666-1 cells showed obviously lowered values of SF2, D0 and Dq but significantly increased α/β with a sensitivity enhancement ratio of 1.4014. COX-2 gene silencing increased the inhibition rate of the tumor xenografts after the radiation, and caused also decreased percentage of G2/M arrest resulting from the exposure.</p><p><b>CONCLUSION</b>Stable COX-2 silencing in NPC cells can improve the effect of radiotherapy both in vitro and in vivo. By changing the radiobiological parameters, genetically based COX-2 inhibitor may be a potentially promising radiosensitizer of NPC.</p>

Effect of gemcitabine in enhancing the radiosensitivity of HepG2 hepatoma cells and the possible mechanism / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the effect of gemcitabine in enhancing the radiosensitivity of hepatoma cell line HepG2 and explore its mechanisms.</p><p><b>METHODS</b>Clonogenic 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.</p><p><b>RESULTS</b>The 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.</p><p><b>CONCLUSION</b>Gemcitabine can significantly enhance the radiosensitivity of HepG2 cells by enhancing radiation-induced cell cycle arrest in G0/G1 phase and cell apoptosis.</p>