HPIP基因沉默抑制肺癌细胞中转化生长因子-β1诱导的上皮-间质转化。
HPIP silencing inhibits TGF-β1-induced EMT in lung cancer cells.
作者信息
Shi Shaomin, Zhao Jianjun, Wang Jing, Mi Donghui, Ma Zhongsen
机构信息
Department of Respiratory Medicine, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130031, P.R. China.
Department of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
出版信息
Int J Mol Med. 2017 Feb;39(2):479-483. doi: 10.3892/ijmm.2017.2851. Epub 2017 Jan 5.
Epithelial-mesenchymal transition (EMT) has been reported to play an important role in the migration and invasion of tumor cells. Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) has emerged as an important regulator of the development of cancer. However, the role of HPIP in lung cancer is unclear. Thus, in the present study, we investigated the role of HPIP in transforming growth factor (TGF)-β1-induced EMT in A549 lung cancer cells in vitro. Our data demonstrated that HPIP was overexpressed in the lung cancer cell lines. TGF-β1 increased the expression of HPIP in the A549 cells. In addition, HPIP silencing significantly attenuated TGF-β1-induced EMT and migration/invasion in the A549 cells. Furthermore, knockdown of HPIP greatly inhibited TGF-β1-induced phosphorylation of Smad2 in the A549 cells. In conclusion, we demonstrated that HPIP silencing suppressed TGF-β1-induced EMT in lung cancer cells by inhibiting Smad2 activation. Therefore, HPIP may be a new therapeutic target for the treatment of lung cancer.
据报道，上皮-间质转化（EMT）在肿瘤细胞的迁移和侵袭中起重要作用。造血前B细胞白血病转录因子（PBX）相互作用蛋白（HPIP/PBXIP1）已成为癌症发展的重要调节因子。然而，HPIP在肺癌中的作用尚不清楚。因此，在本研究中，我们在体外研究了HPIP在转化生长因子（TGF）-β1诱导的A549肺癌细胞EMT中的作用。我们的数据表明，HPIP在肺癌细胞系中过表达。TGF-β1增加了A549细胞中HPIP的表达。此外，HPIP沉默显著减弱了TGF-β1诱导的A549细胞的EMT以及迁移/侵袭。此外，敲低HPIP极大地抑制了TGF-β1诱导的A549细胞中Smad2的磷酸化。总之，我们证明HPIP沉默通过抑制Smad2激活来抑制TGF-β1诱导的肺癌细胞EMT。因此，HPIP可能是治疗肺癌的新治疗靶点。
Zotero 插件