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.