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EMP-1 promotes tumorigenesis of NSCLC through PI3K/AKT pathway
  • ISSN号:1672-0733
  • 期刊名称:Journal of Huazhong University of Science and Tech
  • 时间:2012.12.12
  • 页码:834-838
  • 分类:R734.2[医药卫生—肿瘤;医药卫生—临床医学]
  • 作者机构:[1]Cancer Research Institute, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
  • 相关基金:supported by grants from the National Natural Science Foundation of China (Nos.81072431,30872472,30973496 and 30800569);the Innovative Foundation of Huazhong University of Science and Technology (No.2010MS027);the Foundation of “973” Program (No.2009CB521802);by Special Fund for Central University Basic Scientific Research (Nos.2011JC062,2011JC063)
  • 相关项目:p55PIK对LPS应答的调节及其分子机制
中文摘要:

This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and immunohis to chemically detected to evaluate the correlation of EMP-1 expression to the clinical features of NSCLC. Recombinant adenovirus was constructed to over-express EMP-1 and then infect PC9 cells. Cell proliferation was measured by Ki67 staining. Western blotting was performed to examine the effect of EMP-1 on the PI3K/AKT signaling. Moreover, tumor xeno-grafts were established by subcutaneous injection of PC9 cell suspension (about 5×107/mL in 100 μL of PBS) into the right hind limbs of athymic nude mice. The results showed EMP-1 was significantly up-regulated in NSCLC patients as compared with those with benign lung diseases. Over-expression of EMP-1 promoted proliferation of PC9 cells, which coincided with the activation of the PI3K/AKT pathway. EMP-1 promoted the growth of xenografts of PC9 cells in athymic nude mice. It was concluded that EMP-1 expression may contribute to the development and progress of NSCLC by activating PI3K/AKT pathway.

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期刊信息
  • 《华中科技大学学报:医学英德文版》
  • 主管单位:
  • 主办单位:华中科技大学
  • 主编:
  • 地址:武汉硚口区航空路13号同济医科大学内
  • 邮编:430030
  • 邮箱:
  • 电话:027-83692514
  • 国际标准刊号:ISSN:1672-0733
  • 国内统一刊号:ISSN:42-1679/R
  • 邮发代号:38-56
  • 获奖情况:
  • 国内外数据库收录:
  • 美国化学文摘(网络版),荷兰文摘与引文数据库,美国生物医学检索系统,美国剑桥科学文摘,美国科学引文索引(扩展库)
  • 被引量:597