JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2016, Vol. 54 ›› Issue (11): 7-12.doi: 10.6040/j.issn.1671-7554.0.2016.227

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Mechanical function of HIPK2 in epithelial-mesenchymal transition and metastasis of non-small cell lung cancer

ZHENG Hui, WEI Guangwei   

  1. Department of Anatomy, School of Medicine, Shandong University, Jinan 250012, Shandong, China
  • Received:2016-03-07 Online:2016-11-10 Published:2016-11-10

Abstract: Objective To investigate the role of homeodomain interacting protein kinase 2(HIPK2)in epithelial-mesenchymal transition(EMT)and metastasis in non-small cell lung cancer(NSCLC)cells, and to explore the possible mechanism. Methods The A549 and H520 cells were divided into high expression group and control group, then transfected with pcDNA3.1-HIPK2 and pcDNA3.1-Vector with Lipofectamine 2000. HIPK2 silenced and control cell lines were constructed in A549 by the transfection of GV248 shHIPK2 and GV248 shVector with lentivirus. GV248 shZEB1 and GV248 shVector were transfected with Lipofectamine 2000 in A549 cells in which HIPK2 was silenced. The expression of HIPK2 and EMT markers were detected by Western blotting. The migration and invasion ability of cells were detected through wound scratch assay, Transwell assay and Matrigel assay. Results Compared with control group, the expression of epithelial cell markers in high expression group were enhanced(P<0.01), and the expression of mesenchymal cell markers were descended(P<0.01), which repressed the EMT process. Meanwhile, wound scratch assay showed that the migrated distance of high expression group were less than the control group(P<0.05). Transwell assay and Matrigel assay showed that the number of cells that migrated and invaded through the membrane were obviously 山 东 大 学 学 报 (医 学 版)54卷11期 -郑荟,等.HIPK2抑制非小细胞肺癌上皮间质转化及迁移侵袭的作用及机制 \=-less than those in control group(P<0.01). Conversely, silencing HIPK2 generated the opposite effects. The enhanced EMT and metastasis induced by HIPK2 silencing could be reversed by interfering zinc finger E-box binding homeobox 1(ZEB1). Conclusion HIPK2 represses EMT, migration and invasion of NSCLC cells, and the possible mechanism is related to transcription factor ZEB1.

Key words: Carcinoma, non-small cell lung, Epithelial-mesenchymal transition, Homeodomain interacting protein kinase 2, Migration, Invasion

CLC Number: 

  • R734.2
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