期刊文献+

肺癌细胞中PAK1的表达下调抑制肺癌细胞的增殖和侵袭能力 被引量:2

Downregulated PAK1 expression inhibits NSCLC cells' proliferation and invasion
原文传递
导出
摘要 目的探讨P21激活激酶1(PAK1)在非小细胞肺癌(NSCLC)组织中的表达及其对NSCLC细胞增殖和侵袭能力的影响。方法采用免疫组化和Western blot(WB)方法检测正常肺组织及NSCLC组织中PAK1的蛋白表达水平。利用PAK1-siRNA下调肺癌细胞系A549和LK-2中PAK1的表达后,通过MTT和Transwell等实验方法,明确PAK1对NSCLC细胞增殖和侵袭能力的影响。结果与正常肺组织相比,PAK1在肺癌组织中呈现明显的胞浆强表达,并且其异常表达与肺癌组织的TNM分期(P=0.020)、组织类型(P=0.007)和淋巴结转移相关(P=0.040)。肺癌细胞系中,PAK1的表达下调能够明显抑制肺癌细胞的侵袭和增殖能力(P<0.05)。结论 PAK1促进肺癌细胞的增殖及侵袭能力,发挥着重要的促癌基因功能。 Objective To explore the expression of p21-activated kinase 1(PAK1) in non-small-cell lung cancer (NSCLC) tissue and its effects on the proliferation and migration of non-small-cell lung cancer cells. Methods Immunohistochemistry and Western blot were used to detect the expression of PAK1 in normal lung tissues and NSCLC tissues. The proliferationand invasion of lung cancer cells were detected by MTT and transwell. Results Compared with normal lung tissues, PAK1 was strongly expressed in the cytoplasm of lung cancer tissues, and its abnormal expression was correlated with the TNM stage of lung cancer tissues (p = 0.020), histological types (p = 0.007) and lymph node metastasis (p = 0.040). In lung cancer cell lines, down-regulation of PAK1 expression could significantly inhibited the invasion and proliferation of lung cancer cells. Conclusion PAK1 plays an important role in promotingcarcinogenesisby enhancing the proliferation and invasion of Lung Cancer Cells.
作者 孙瑞泽 王思尧 姜贵洋 徐洪涛 王恩华 刘洋 SUN Rui-ze;WANG Si-yao;JIANG Gui-yang;XU Hong-tao;WANG En-hua;LIU Yang(Department of Pathology, the Basic Medical Sciences, China Medical University, Shenyang 110122, China;Department of Pharmaceutical Biotechnology, the Queen's University of Belfast Joint College, China Medical University, Shenyang 110122, China)
出处 《解剖科学进展》 2019年第2期113-117,共5页 Progress of Anatomical Sciences
基金 国家自然科学基金(81772489) 辽宁省教育厅基金(L2015583) 辽宁省科技厅自然科学基金(20180530045)
关键词 非小细胞肺癌 p21激活激酶1 细胞增殖 细胞侵袭 NSCLC p21-activated kinase 1 cell proliferation cell invasion
  • 相关文献

参考文献1

二级参考文献1

共引文献6

同被引文献20

引证文献2

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部