Correlation between oncogene integrator complex subunit 7 and a poor prognosis in lung adenocarcinoma

癌基因整合复合物亚基7与肺腺癌预后不良的相关性

阅读:10
作者:Zhoubin Li # ,Pengwei Zhu # ,Maoling Wang ,Cheng Fang ,Huafeng Ji

Abstract

Background: Lung adenocarcinoma (LUAD) is one of the most common types of cancer worldwide with high incidence and mortality rates. The integrator complex subunit 7 (INTS7) encodes a subunit of the integrator complex that mediates small-nuclear ribonucleic acid (RNA) processing and has been shown to be associated with RNA polymerase II. However, the clinical significance of INTS7 in LUAD is still not clear and needs to be investigated. Methods: The single-cell sequencing of a publicly available data set was conducted to compare the expression levels and percentages of INTS7 in lung malignant cells at different classifications and stages. Further, 33 cancer types from The Cancer Genome Atlas (TCGA) database were analyzed, protein-protein interaction (PPI) networks were constructed, and functional annotations were undertaken for the INTS7 gene. INTS7 small-interfering RNAs were transfected into LUAD cell lines, and cell biological behaviors, such as migration, invasion, apoptosis and proliferation capacity, were then examined. Results: We found that the expression of INTS7 was significantly more upregulated in the LUAD tissues than the adjacent normal tissues. Increased INTS7 messenger RNA expression was correlated with TNM (tumor node metastasis classification) stage and gender in LUAD patients. Further, the Kaplan-Meier survival analysis indicated that LUAD patients with high INTS7 expression levels had a worse prognosis than those with low INTS7 expression levels. Finally, we found that silencing INTS7 inhibited LUAD cell viability and invasion in vitro. Conclusions: These results suggest that INTS7 can be used as a potential therapy target and prognostic marker for LUAD. Further, INTS7 may aggravate migration and invasion, induce the proliferation, and attenuate the apoptosis capacity of cells in LUAD.

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。