期刊
ONCOTARGET
卷 7, 期 24, 页码 36489-36500出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9269
关键词
ISL1; gastric cancer; proliferation; CCNB; c-MYC
资金
- National Natural Science Foundation of China [81071675, 81370236, 81371889, 81472022]
- Natural Science Foundation of Beijing [5122021]
- Leading Academic Discipline Project of Beijing Education Bureau
- 111 Project of China [B07001]
Islet-1 (ISL1) belongs to the LIM homeodomain transcription factor family, which is specifically expressed in certain tissue types only. Previously, we reported that ISL1 is aberrantly overexpressed in gastric cancer (GC). However, its role in GC is not clear. Here, we report that ISL1 is aberrantly upregulated not only in human gastric carcinoma tissues but also in some GC cell lines. Upregulated ISL1 expression enhanced xenografted gastric carcinoma development, while ISL1 knockdown inhibited GC growth in nude mice. ISL1 overexpression promoted GC cell proliferation, colony formation, and cell growth in soft agar, and facilitated cell cycle transition in GC cells, demonstrated an increase in the proportion of cells in the G(2)/M and S phases and a decrease in the proportion of cells in the G(1) phase. Furthermore, we provide evidence that ISL1 is a novel regulator of the cyclin B1 (CCNB1), cyclin B2 (CCNB2) and c-myc (c-MYC) genes. ISL1 activated the expression of these genes in GC cells by binding to the conserved binding sites on their promoters or enhancers. The expression levels of the genes were decreased in response to ISL1 knockdown. Therefore, ISL1 may serve as a potential therapeutic target in GC.
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