结直肠癌
癌变
癌症研究
细胞生长
生物标志物
癌症
转录因子
生物
基因
医学
内科学
遗传学
作者
Jing Tang,Lirui Yang,Yafei Li,Xuelian Ning,Anita Chaulagain,Tianzhen Wang,Dong Wang
出处
期刊:Carcinogenesis
[Oxford University Press]
日期:2020-11-09
卷期号:42 (4): 578-586
被引量:33
标识
DOI:10.1093/carcin/bgaa118
摘要
Abstract Colorectal cancer (CRC) is one of the most common malignant tumours, and its morbidity and mortality rates are relatively high. However, the aetiology and pathogenesis of CRC have not been clearly elucidated to date. AT-rich interaction domain 3A (ARID3A) is a member of the ARID3 family and a transcription factor that can bind to specific DNA sites to regulate gene expression. It was reported that ARID3A is involved in various biological processes and may be related to carcinogenesis. In this study, by assessing the mRNA level of ARID3A in TCGA database, we found that ARID3A expression increased in CRC tissues, and proposed that ARID3A could act as a tumour-promoting factor in the development of CRC. To verify this hypothesis, we used cell proliferation, migration and invasion assays to assess the effect of ARID3A on CRC cells. We revealed that ARID3A overexpression enhanced tumour cell proliferation, migration and invasion. ARID3A could target Aurora kinase A (AURKA) to facilitate the malignant phenotype of CRC cells, and patients with a higher ratio of AURKA and ARID3A had a better overall survival. Conclusively, this study showed that ARID3A targeted AURKA to facilitate the development of CRC. The ratio of ARID3A and AURKA could be used as a potential biomarker to predict prognosis, providing a new strategy for the diagnosis and prognosis of CRC.
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