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siRNA干扰微管微丝交连因子1表达增强替莫唑胺诱导的胶质瘤细胞毒性

谢思迪 陈子阳 王海 何敏毅 陆云涛 雷炳喜 李和珍 刘亚伟 漆松涛

南方医科大学学报2017,Vol.37Issue(9):1183-1189,7.
南方医科大学学报2017,Vol.37Issue(9):1183-1189,7.DOI:10.3969/j.issn.1673-4254.2017.09.07

siRNA干扰微管微丝交连因子1表达增强替莫唑胺诱导的胶质瘤细胞毒性

MACF1 knockdown in glioblastoma multiforme cells increases temozolomide-induced cytotoxicity

谢思迪 1陈子阳 1王海 2何敏毅 1陆云涛 3雷炳喜 1李和珍 4刘亚伟 5漆松涛1

作者信息

  • 1. 南方医科大学南方医院神经外科,广东广州510515
  • 2. 广州医科大学第六医院神经外科,广东广州511500
  • 3. 南方医科大学南方医院临床医学教育中心,广东广州510515
  • 4. 中山大学孙逸仙纪念医院神经外科,广东广州510000
  • 5. 南方医科大学第五附属医院神经外科,广东广州510900
  • 折叠

摘要

Abstract

Objective To investigate the role of microtubule-actin crosslinking factor 1 (MACF1) in the response of glioma cells to temozolomide (TMZ).Methods TMZ was applied to a human gliomablastoma cell line (U87) and changes in the protein expression and cellular localization were determined with Western blot,RT-PCR,and immunofluorescence.The responses of the cells with MACF1 expression knockdown by RNA interference to TMZ were assessed.TMZ-induced effects on MACF1 expression were also assessed by immunohistochemistry in a nude mouse model bearing human glioblastoma xenografts.Results TMZ resulted in significantly increased MACF1 expression (by about 2 folds) and changes in its localization in the gliomablastoma cells both in vitro and in vivo (P<0.01).Knockdown of MACF1 reduced the proliferation (by 45%) of human glioma cell lines treated with TMZ (P<0.01).TMZ-induced changes in MACF1 expression was accompanied by cytoskeletal rearrangement.Conclusion MACF1 may be a potential therapeutic target for glioblastoma.

关键词

细胞骨架/微管微丝交连因子1/胶质母细胞瘤/替莫唑胺

Key words

cytoskeleton rearrangement/microtubule-actin crosslinking factor 1/temozolomide/glioblastoma multiforme

引用本文复制引用

谢思迪,陈子阳,王海,何敏毅,陆云涛,雷炳喜,李和珍,刘亚伟,漆松涛..siRNA干扰微管微丝交连因子1表达增强替莫唑胺诱导的胶质瘤细胞毒性[J].南方医科大学学报,2017,37(9):1183-1189,7.

基金项目

国家自然基金(81372692,81302229,81472315) (81372692,81302229,81472315)

广东省自然科学基金(2014A030313167) (2014A030313167)

高校博士学科点专项科研基金(20134433120014) (20134433120014)

国家临床重点专科建设项目经费资助 ()

Supposed by National Natural Science Foundation of China (81372692,81302229,81472315). (81372692,81302229,81472315)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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