临床肿瘤学杂志
臨床腫瘤學雜誌
림상종류학잡지
CHINESE CLINICAL ONCOLOGY
2014年
7期
584-588
,共5页
孟庆红%孙新臣%孙苏平%于静萍%倪新初%赵迪
孟慶紅%孫新臣%孫囌平%于靜萍%倪新初%趙迪
맹경홍%손신신%손소평%우정평%예신초%조적
纳米Fe3 O4/C225复合物%人结直肠癌%放疗增敏%表皮生长因子受体
納米Fe3 O4/C225複閤物%人結直腸癌%放療增敏%錶皮生長因子受體
납미Fe3 O4/C225복합물%인결직장암%방료증민%표피생장인자수체
Nano Fe3 O4/C225 complex%Human colorectal cancer%Radiosensitivity%Epidermal growth factor receptor
目的:探讨纳米Fe3 O4/C225复合物(简称复合物)对结直肠癌LoVo细胞放射增敏性的影响。方法采用MTT法观察不同浓度复合物(0、3?125、6?25、12?5、25、50、100mg/L)作用24h后的增殖抑制率,根据实验设计分为单纯照射组、C225+照射组及复合物+照射组,采用克隆形成实验检测3组经0、2、4、6、8和10Gy X线照射后的存活分数( SF),流式细胞仪检测3组经4Gy X线照射24h后的细胞周期情况,采用Western blotting检测经4Gy X线照射24h后的表皮生长因子受体( EGFR)蛋白水平及其相关信号通路中p-P38和p-Akt蛋白水平。结果在3?125~100mg/L范围内,随复合物浓度增加, LoVo细胞的增殖抑制率升高,0、3?125、6?25、12?5、25、50、100mg/L的增殖抑制率依次为0%、(8?950±0?086)%、(14?760±0?011)%、(29?860±0?001)%、(41?750±0?017)%、(59?770±0?010)%和(78?710±0?017)%,组间差异有统计学意义(P<0?05);复合物+照射组的SF、S期细胞比例及p-Akt、EGFR蛋白水平均低于C225+照射组和单纯照射组,G0/G1期、G2/M期细胞比例及p-P38蛋白水平均高于C225+照射组和单纯照射组,以上差异均有统计学意义( P<0?05)。结论纳米Fe3 O4/C225复合物可抑制LoVo细胞增殖并具有放射增敏作用,可能与G0/G1期阻滞及EGFR相关信号通路受抑制有关。
目的:探討納米Fe3 O4/C225複閤物(簡稱複閤物)對結直腸癌LoVo細胞放射增敏性的影響。方法採用MTT法觀察不同濃度複閤物(0、3?125、6?25、12?5、25、50、100mg/L)作用24h後的增殖抑製率,根據實驗設計分為單純照射組、C225+照射組及複閤物+照射組,採用剋隆形成實驗檢測3組經0、2、4、6、8和10Gy X線照射後的存活分數( SF),流式細胞儀檢測3組經4Gy X線照射24h後的細胞週期情況,採用Western blotting檢測經4Gy X線照射24h後的錶皮生長因子受體( EGFR)蛋白水平及其相關信號通路中p-P38和p-Akt蛋白水平。結果在3?125~100mg/L範圍內,隨複閤物濃度增加, LoVo細胞的增殖抑製率升高,0、3?125、6?25、12?5、25、50、100mg/L的增殖抑製率依次為0%、(8?950±0?086)%、(14?760±0?011)%、(29?860±0?001)%、(41?750±0?017)%、(59?770±0?010)%和(78?710±0?017)%,組間差異有統計學意義(P<0?05);複閤物+照射組的SF、S期細胞比例及p-Akt、EGFR蛋白水平均低于C225+照射組和單純照射組,G0/G1期、G2/M期細胞比例及p-P38蛋白水平均高于C225+照射組和單純照射組,以上差異均有統計學意義( P<0?05)。結論納米Fe3 O4/C225複閤物可抑製LoVo細胞增殖併具有放射增敏作用,可能與G0/G1期阻滯及EGFR相關信號通路受抑製有關。
목적:탐토납미Fe3 O4/C225복합물(간칭복합물)대결직장암LoVo세포방사증민성적영향。방법채용MTT법관찰불동농도복합물(0、3?125、6?25、12?5、25、50、100mg/L)작용24h후적증식억제솔,근거실험설계분위단순조사조、C225+조사조급복합물+조사조,채용극륭형성실험검측3조경0、2、4、6、8화10Gy X선조사후적존활분수( SF),류식세포의검측3조경4Gy X선조사24h후적세포주기정황,채용Western blotting검측경4Gy X선조사24h후적표피생장인자수체( EGFR)단백수평급기상관신호통로중p-P38화p-Akt단백수평。결과재3?125~100mg/L범위내,수복합물농도증가, LoVo세포적증식억제솔승고,0、3?125、6?25、12?5、25、50、100mg/L적증식억제솔의차위0%、(8?950±0?086)%、(14?760±0?011)%、(29?860±0?001)%、(41?750±0?017)%、(59?770±0?010)%화(78?710±0?017)%,조간차이유통계학의의(P<0?05);복합물+조사조적SF、S기세포비례급p-Akt、EGFR단백수평균저우C225+조사조화단순조사조,G0/G1기、G2/M기세포비례급p-P38단백수평균고우C225+조사조화단순조사조,이상차이균유통계학의의( P<0?05)。결론납미Fe3 O4/C225복합물가억제LoVo세포증식병구유방사증민작용,가능여G0/G1기조체급EGFR상관신호통로수억제유관。
Objective To investigate the radiosensitivity enhancement and possible mechanism of nano Fe3 O4/C225 complex on human colorectal cancer LoVo cells. Methods In vitro inhibition rates of cell proliferation at 24h after treatment with different con-centrations (0, 3?125, 6?25, 12?5, 25, 50, 100 mg/mL) of nano Fe3O4/C225 complex were determined by MTT. According to the experimental protocol, the below experiments were carried out in irradiation group, C225+irradiation group and complex+irradiation group. The colony formation assay was employed to observe the surviving fraction ( SF) of three groups after X-ray irradiation of 0, 2, 4, 6, 8, 10Gy. The cell cycle of three groups at 24h after X-ray irradiation of 4Gy was measured by flow cytometry. Western blotting was employed to measure the protein level of epidermal growth factor receptor ( EGFR) and p-P38, p-Akt in the related of signaling pathway. Results The proliferation inhibition rate of LoVo cells gradually increased with the increasing concentration of Fe3 O4/C225 complex ranging from 3?125 to 100 mg/L. The proliferation inhibition rates were 0%, (8?950± 0?086)%, (14?760± 0?011)%, (29?860± 0?001)%, (41?750± 0?017)%, (59?770± 0?010)% and (78?710± 0?017)% at the concentrations of 0, 3?125, 6?25, 12?5, 25, 50, 100mg/mL with statistically significant differences ( P<0?05) . Compared with irradiation group and C225+irradiation group, there were lower SF, percentage of S cells and protein levels of p-Akt, EGFR and higher percentages of G0/G1 and G2/M and protein level of p-P38 in complex+irradiation group with statistically significant differences (P<0?05). Conclusion Nano Fe3O4/C225 complex could inhibit the proliferation of LoVo cells with radiosensitizing effect possibly via the arrest at the G0/G1 phase and in-hibition of EGFR signaling pathways.