Expression of DCUN1D1 in laryngeal squamous cell carcinoma and its inhibiting effect on TU-177 cells after interfered by RNA

DCUN1D1在喉鳞状细胞癌中的表达及RNA干扰对TU-177细胞的抑制作用

阅读:19
作者:Jing Liu, Yu Shuang, Chao Li, Xuan Zhou, Yongwang Huang, Lun Zhang

Abstract

Expression of DCUN1D1 in laryngeal squamous cell carcinoma (LSCC) and its inhibition by small interfering RNA (siRNA) target in the TU-177 cells was investigated. Immunohistochemistry was used to detect the expression level of DCUN1D1 in LSCC tissue in 140 cases and to analyze its relationship with clinical pathological characteristics. siRNA expression plasmid targeting DCUN1D1 was constructed and transferred into TU-177 cells. The effect of siRNA target DCUN1D1 gene silencing on proliferation, invasion and migration of TU-177 cells were observed by MTS assay and Transwell experiment. The expression levels of focal adhesion kinase (FAK) and matrix metalloproteinase-2(MMP-2) were detected by western blot. Expression level of DCUN1D1 protein increased significantly in T3 + T4, N+, and III + IV stages of LSCC patients (P < .05). After DCUN1D1 was targeted by siRNA, the DCUN1D1 protein level decreased 67% in siRNA-3 group, where average absorbance value was lower than the control and blank group with significant difference(F = 6.076, P < .05) in MTS assay, meantime migration, and invasion cells in each vision were the same (F = 19.851, F = 25.454, P < .01) in the Transwell experiment. The expression level of FAK and MMP-2 was significantly down-regulated in siRNA-3 group (F = 28.896, F = 40.240, P < .01). DCUN1D1 is associated with progression and prognosis of LSCC. After siRNA based target on DCUN1D1, TU-177 cells growth was inhibited and invasion of malignant tumour was diminished by reducing the expression of FAK and MMP-2. DCUN1D1 is could become a potential new target for the treatment of LSCC.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。