Aurora-A促进胰腺癌细胞放射抵抗的机制研究

孙会贞; 杨恭

doi:10.3969/j.issn.1007-3969.2013.12.007

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Aurora-A促进胰腺癌细胞放射抵抗的机制研究

更新时间：2025-12-31

- Aurora-A促进胰腺癌细胞放射抵抗的机制研究
- Mechanistic study of pancreatic cancer cell radioresistance conferred by Aurora-A
- 中国癌症杂志 2013年23卷第12期页码：974-979
- 作者机构：
  
  复旦大学附属肿瘤医院实验研究中心，复旦大学上海医学院肿瘤学系,上海,200032
- 作者简介：
- 基金信息：
  
  浦江人才计划基金(No：PJ[2011]0000652)
- DOI：10.3969/j.issn.1007-3969.2013.12.007
  中图分类号：
- 网络出版：2014-02-17，
  
  纸质出版：2013-02-17
- 稿件说明：
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孙会贞,杨恭. Aurora-A促进胰腺癌细胞放射抵抗的机制研究[J]. 中国癌症杂志, 2013, 23(12): 974-979.

孙会贞, 杨恭. Mechanistic study of pancreatic cancer cell radioresistance conferred by Aurora-A[J]. China Oncology, 2013, 23(12): 974-979.
孙会贞,杨恭. Aurora-A促进胰腺癌细胞放射抵抗的机制研究[J]. 中国癌症杂志, 2013, 23(12): 974-979. DOI： 10.3969/j.issn.1007-3969.2013.12.007.

孙会贞, 杨恭. Mechanistic study of pancreatic cancer cell radioresistance conferred by Aurora-A[J]. China Oncology, 2013, 23(12): 974-979. DOI： 10.3969/j.issn.1007-3969.2013.12.007.

摘要

背景与目的：Aurora-A属于丝氨酸和苏氨酸蛋白激酶家族，其异常表达可导致肿瘤发生及其对放射线的抵抗，本研究旨在探讨Aurora-A与细胞放射敏感的相关性。方法：用Aurora-A激酶抑制剂处理Capan-1细胞，检测细胞增殖、锚定非依赖性生长和细胞周期及其周期相关蛋白的变化；处理的细胞同时用γ线照射，然后用流式细胞术检测细胞凋亡。结果：Aurora-A激酶抑制剂处理后，Capan-1细胞生长速度减慢，克隆形成率降低；Aurora-A抑制可引起细胞周期G

/S以及G

/M期转化阻滞，Cyclin D1、CDK2和CDK6表达下降。Aurora-A激酶抑制剂处理后可以提高放射线照射诱导的细胞凋亡率。结论：Aurora-A激酶抑制剂可抑制胰腺癌细胞增殖，阻滞细胞周期，促进细胞对放射线照射的敏感性。因此，Aurora-A可能是胰腺癌放射治疗增敏的靶向分子之一。

Abstract

Background and purpose: Aurora-A is a member of serine/threonine kinase family. The abnormal expression of Aurora-A induces tumorigenesis and radioresistance. This study was aimed to investigate the association of Aurora-A with radioresistance. Methods: Capan-1 cells were treated with Aurora-A kinase inhibitor

and then used to test cell proliferation

anchorage independent assay

cell cycle

and cell cycle regulatory proteins. Treated cells were also used to detect cell apoptosis after γ-irradiation. Results: Cell growth and colony number in soft agar were decreased after treatment with Aurora-A inhibitor. Treatment of cells with Aurora-A inhibitor also down-regulated the expression of Cyclin D1

CDK2 and CDK6 to induce cell cycle arrest at G

/S and G

/M phases

but promoted cell apoptosis a

fter γ-irradiation. Conclusion: Treatment of pancreatic cancer cells with Aurora-A kinase inhibitor blocks cell proliferation and cell cycle progression

and promotes sensitivity of cells to radiation. Thus

Aurora-A may be used as one of therapeutic targets to increase the sensitivity of pancreatic cancer radiotherapy.

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