[1]仲钰婕,尤为,赵梦洁,等.抑制ROCKⅡ下调丝切蛋白1表达提高胶质瘤细胞的放射敏感性[J].临床神经外科杂志,2019,16(5):420-424.[doi:10.3969/j.issn.1672-7770.2019.05.011]
 ZHONG Yu-jie,YOU Wei,ZHAO Meng-jie,et al.Improve U251 glioma cell radiosensitivity and down-regulate cofilin1 via inhibiting ROCKⅡ[J].Journal of Clinical Neurosurgery,2019,16(5):420-424.[doi:10.3969/j.issn.1672-7770.2019.05.011]
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抑制ROCKⅡ下调丝切蛋白1表达提高胶质瘤细胞的放射敏感性()
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《临床神经外科杂志》[ISSN:1672-7770/CN:32-1727/R]

卷:
16
期数:
2019年第5期
页码:
420-424
栏目:
论著
出版日期:
2019-10-15

文章信息/Info

Title:
Improve U251 glioma cell radiosensitivity and down-regulate cofilin1 via inhibiting ROCKⅡ
作者:
仲钰婕尤为赵梦洁肖勇王臻王冉冉钱春发胡新华刘宏毅肖红
210029 南京,南京医科大学附属脑科医院研究所(仲钰婕,赵梦洁,王冉冉,肖红),神经外科(肖勇,王臻,钱春发,胡新华,刘宏毅);南京医科大学康达医学院临床医学系(尤为)
Author(s):
ZHONG Yu-jie YOU Wei ZHAO Meng-jie et al.
Department of Neuro-Psychiatric Institute, the Brain Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China
关键词:
胶质瘤放射敏感性丝切蛋白1ROCKⅡU251细胞
Keywords:
glioma radiosensitivity cofilin1 ROCKⅡ U251 cells
分类号:
R739.41
DOI:
10.3969/j.issn.1672-7770.2019.05.011
文献标志码:
A
摘要:
【摘要】目的 研究丝切蛋白1(cofilin1,CFL1)介导放射抵抗性的潜在机制,探讨CFL1的上游调控元件与人脑胶质瘤细胞经放疗后细胞活力的关系。方法抑制Rho相关卷曲螺旋蛋白激酶Ⅱ(Rho-associated coiled-coil forming proteinkinase,ROCKⅡ)后,测定正常U251细胞及放射抵抗性U251(RR-U251)细胞CFL1蛋白的表达水平;并通过放射治疗后细胞的增殖、侵袭和迁移实验,评估其放射敏感性。结果通过抑制ROCKⅡ,RR-U251细胞的增殖、迁移和侵袭能力均明显降低,放射敏感性得到显著提高。结论ROCKⅡ为CFL1介导放射抵抗性的表型之一;其为进一步提高临床放射治疗的效果提供了潜在的生物标志物。
Abstract:
Abstract: ObjectiveTo clarify the potential mechanism of CFL1-mediated radioresistance and the association of CFL1 upstream regulators with cell motility after irradiation in human glioma cells. MethodsAfter inhibiting ROCKⅡ, the alteration of radiosensitivity and CFL1 expression level in both normal U251 and radioresistant U251(RR-U251) cells were respectively evaluated. The cell radiosensitivity was assessed through cell vitality, invasion and migration experiments after irradiation. ResultsThe results showed that the cell vitality, migration and invasion capabilities of RR-U251 cells significantly decreased with radiosensitivity significantly improved via inhibiting ROCKⅡ. Down-regulation of ROCKⅡ could simultaneously decrease CFL1 level in glioma cells. ConclusionThe present study indicates the involvement of ROCKⅡ in CFL1-mediated radioresistant phenotype and provides potential biomarkers for improvement of further clinical radiotherapy.

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更新日期/Last Update: 2019-10-15