期刊文献+

EGFR/AKT信号转导通路在调控结肠癌LoVo细胞生物学行为中的作用研究 被引量:1

Role of EGFR/AKT Pathway on the Biological Behavior of Human Colon Cancer Cells
原文传递
导出
摘要 目的:探讨EGFR/AKT(表皮生长因子受体/蛋白激酶B)信号转导通路在调控人结肠癌细胞株LoVo生物学行为中的作用机制方法:用EGFR抑制剂AG1478处理人结肠癌细胞LoVo;用免疫细胞化学法检测p-EGFR及p-AKT蛋白表达;用MTT法检测细胞的增殖;用流式细胞仪检测细胞的凋亡水平;用Transwell小室观察体外细胞迁移能力;用Transwell小室结合Matrigel胶检测肿瘤细胞侵袭能力结果:AG1478(20μmol/L)处理后,p-EGFR及p-AKT的表达水平明显降低(P<0.05),细胞的增殖、迁移和侵袭能力明显下降(P<0.05),细胞凋亡水平明显提高(P<0.05)。结论:EGFR与人结肠癌细胞LoVo的增殖、凋亡、迁移和侵袭性密切相关,并可能通过AKT信号转导通路调控人结肠癌的发展。 Objective: To investigate the mechanism of epidermal growth factor receptor(EGFR)/Protein kinase B(PKB or AKT) signaling pathway on biological behavior of human colon cancer cell LoVo. Methods: LoVo cells were treated with AG1478. The expression of EGFR and AKT was detected by western blotting in LoVo cells. Cell proliferation assay and Matrixgel were used to examine the capability of proliferation, migration and invasion. FCM was used to examine the capability ofapoptosis. Results: After the treatment of AG 1478(20μmol/L), the expression of p-EGFR and p-AKT were decreased remarkably (P〈0.05). AG1478 inhibited significantly the capability of proliferation, migration and invasion in LoVo cells (P〈0.05). The capability ofapoptosis was markedly improved (P〈0.05). Conclusion: EGFR might play a key role on the capability of proliferation, apoptosis, migration and invasion in human colon cancer cell line LoVo. It could be partly related to the mechanism of AKT signaling pathway.
出处 《现代生物医学进展》 CAS 2009年第3期440-443,F0003,共5页 Progress in Modern Biomedicine
基金 国家自然科学基金资助项目(30400534)
关键词 EGFR/AKT信号转导通路 AG1478 细胞增殖 细胞凋亡 细胞迁移 细胞侵袭 EGFR/AKT signaling pathway AG1478 LoVo cells Proliferation Apoptosis Migration Invasion
  • 相关文献

参考文献13

  • 1Herbst RS. Review of epidermal growth factor receptor biology [J]. Int J Radiat Oncol Biol Phys, 2004, 59(2Suppl): 21-26
  • 2Testa JR, Bellacosa A. AKT plays a central role in tumorigenesis [J]. Proc Natl Acad Sci USA, 2001, 98(20): 10983-10985
  • 3Geng Shu-an. The discussion of the reasons of Colorectal cancer recurrence[J]. Tianjin Medical Journal, 2005, 1(3): 475-476
  • 4Jorissen RN, Walker F, Pouliot N, et al. Epidermal growth factor receptor:mechanisms of activation and signaling [J]. Exp Cell Res, 2003, 284(1): 31-53
  • 5Li J, Kleeff J, Giese N, et al. Gefitinib (‘IRESSA',ZD1839),a selective epidermal growth factor receptor tyrosine kinase inhibitor, inhibits pancreatic cancer cell growth,invasion, and colony formation [J]. Int J Oncol, 2004, 25(1): 203-210
  • 6Krysan K, Reckamp KL, Dalwadi H, et al. ProstaglandinE2 activates mitogen- activated protein kinase /Erk pathway signaling and cell proliferation in non-small cell lung cancer cells in an epidermal growth factor receptor-independent manner [J]. Cancer Res, 2005, 65 ( 14): 6275 -6281
  • 7Raymond E, Faivre S, Armand JP. Epidermal growth factor receptor tyrosine kinase as a target for anticancer therapy [J]. Drugs, 2000, 60 (4):15-23
  • 8Downwrd J. PI 3-kinase, Akt and cell surviva [J]. Semin Cell Dev Biol, 2004, 15 (2): 177-182
  • 9Fujino H, Regan JW. Prostanold receptors and PI 3-kinase: a pathway to cancer [J]?Trends Pharmacol Sci, 2003, 24(2): 335-340
  • 10Zhang L, Jiang L, Sun Q, et al. Prostaglandin E2 enhances mitogen-activated protein kinase/Erk pathway in human cholangiocarcinoma cells: involvement of EP1 receptor, calcium and EGF receptors signaling [J]. Mol Cell Biochem, 2007,305(1-2):19-26

同被引文献97

引证文献1

二级引证文献53

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