Abstract
Great concerns have raised crucial roles of long noncoding RNAs (lncRNAs) on colorectal cancer progression due to the increasing number of studies in cancer development. Previous studies reveal that lncRNA CCAT1 plays an important role in the progression of a variety of cancers. However, the role of lncRNA CCAT1 in colorectal cancer is still unclear. In this study, we found that in both colorectal tissues and cell lines the level of lncRNA CCAT1 was increased. Downregulation of lncRNA CCAT1 inhibited the proliferation, migration, and invasion of colorectal cell lines and promoted apoptosis. We then found that hsa-miR-4679 could bind to lncRNA CCAT1 directly, and with further functional analyses, we confirmed that lncRNA CCAT1 sponged hsa-miR-4679 to promote the progression of colorectal cancer. Next, we found that hsa-miR-4679 was directly bound to 3′UTR of GNG10 (guanine nucleotide-binding protein, gamma 10). GNG10 overexpression promoted the progression of colorectal cancer, and this phenotype could be reversed by miR-4679 mimics. At last, we knocked down CCAT1 in vivo and found that sh-CCAT1 reduced the tumor size and the number of proliferating cells. In summary, our findings revealed that lncRNA CCAT1 facilitated colorectal cancer progression via the hsa-miR-4679/GNG10 axis and provided new potential therapeutic targets for colorectal cancer.
Highlights
Colorectal cancer (CRC), the fourth most deadly cancer in the world, resulting in 900 000 deaths annually, is caused by hereditary and environmental risk factors, including aging, dietary habits of developing countries, obesity, lack of physical exercise, and smoking [1, 2]
We found that long noncoding RNAs (lncRNAs) cancer-associated transcript-1 (CCAT1) promoted the progression of CRC via hsa-miR-4679 mediating the expression of GNG10
We measured the level of lncRNA CCAT1 in human colon immortalized cell line FHC and two colorectal cancer cell lines, HT-29 and HCT-116, and found that lncRNA CCAT1 was upregulated in colorectal cancer cell lines (Figure 1(b))
Summary
Colorectal cancer (CRC), the fourth most deadly cancer in the world, resulting in 900 000 deaths annually, is caused by hereditary and environmental risk factors, including aging, dietary habits of developing countries, obesity, lack of physical exercise, and smoking [1, 2]. Great concerns have been arisen by the increasing number of colorectal cancer patients younger than 50 years, especially rectal cancer and distal colon cancer [3,4,5]. CRC patients respond to the common therapy differently, which may be due to the diverse causes on the cellular and molecular levels [7,8,9]. Multiple molecules regulated the initiation and progression of CRC as a network. The mechanisms underlying the initiation and progression of CRC are still poorly understood
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