基因敲除
癌症研究
生物
转移
癌基因
细胞周期蛋白D1
细胞生长
下调和上调
上皮-间质转换
肿瘤进展
癌症
细胞周期
细胞培养
基因
遗传学
作者
Ying‐Chieh Chen,Chih-Chi Kuo,Chih‐Feng Chian,Ching Tzao,Shan‐Yueh Chang,Yu‐Lueng Shih,Ya‐Wen Lin,Mu-Hsien Yu,Her‐Young Su
标识
DOI:10.1016/j.yexcr.2018.04.011
摘要
The main problem in the treatment of non-small cell lung cancer (NSCLC) is metastasis. Epithelial–mesenchymal transition (EMT) is known as the critical signaling in tumor progression, metastasis, and also the drug resistance. In this study, we reported a novel gene Polymerase delta-interacting protein 2 (POLDIP2) was downregulated in NSCLC tissues and first demonstrated that overexpression of POLDIP2 increased the anchorage-independent growth (AIG) and invasiveness of H1299 cells. In addition, we examined that knockdown of POLDIP2 in H1299 and A549 cells reduced tumorigenicity and metastatic capacity in vitro and also in vivo. Moreover, downregulation of the cell proliferation marker cyclin D1 and EMT markers CDH2, Slug, and Twist was showed in H1299 cells by POLDIP2 knockdown, suggesting that the inhibition of malignancy was affected by modulating key genes for tumor growth and invasiveness. Taken together, our study is the first study that demonstrated that POLDIP2 gene was function as an oncogene in NSCLC and implied the oncogenic ability might be through promoting cell proliferation or EMT.
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