RETRACTED: Relationship between DLK1 gene promoter region DNA methylation and non-small cell lung cancer biological behavior (Retracted article. See vol. 20, pg. 981, 2020)

被引:5
|
作者
Zhong, Zhaokui [1 ]
Ye, Yongting [2 ]
Guo, Wei [1 ]
He, Yi [3 ]
Hu, Weicai [3 ]
机构
[1] Cent Hosp Zhumadian, Dept Thorac Surg, 77 China Rd, Zhumadian 463000, Henan, Peoples R China
[2] Fourth Peoples Hosp Zhumadian, Dept Internal Med, Zhumadian 463000, Henan, Peoples R China
[3] Henan Prov Peoples Hosp, Dept Thorac Surg, Zhengzhou 450003, Henan, Peoples R China
关键词
DLK1; gene; DNA methylation in promoter region; non-small cell lung cancer; invasion ability; Notch; matrix metalloproteinase-9; HYPOMETHYLATION; EXPRESSION; PCR;
D O I
10.3892/ol.2017.6019
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We investigated the possible association between DLKI gene promoter region methylation and the increased invasion capacity of non-small cell lung cancer (NSCLC). Lung cancer cell line H1299, as well as the gene transfection and RNA interference technology were used to build DLK gene overexpression and knockdown cells. An in vitro invasion assay was performed to observe the changes in the invasion ability of lung cancer cells. Western blot analysis was used to verify Notchl and matrix metalloproteinase-9 (MMP-9) expression levels and a sulfurous acid sequencing technique was used to test the DNA methylation level in the promoter region. Our results showed that the invasion ability of cells in the overexpression group was significantly enhanced. This ability was considerably reduced in the knockdown group. The Notchl and MMP-9 expression level increased significantly in the overexpression group, while it was reduced considerably in the knockdown group. We detected significantly lower levels of DNA methylation in the promoter region in the overexpression group. It was concluded that methylation of the DLK1 gene promoter region increased the invasion ability of NSCLC. Furthermore, it is possible that this process is related to the Notch signaling pathway.
引用
收藏
页码:4123 / 4126
页数:4
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