Department of Surgery, School of Clinical Medicine, Dali University, Dali, Yunnan 671000, China.
Department of General Surgery, The First Affiliated Hospital of Dali University, Dali University, Dali, Yunnan 671000, China.
J Immunol Res. 2021 Dec 30;2021:8930813. doi: 10.1155/2021/8930813. eCollection 2021.
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 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.
由于越来越多的研究表明长链非编码 RNA（lncRNA）在癌症发展过程中起着关键作用，因此人们对其在结直肠癌进展中的作用产生了极大的关注。先前的研究表明，lncRNA CCAT1 在多种癌症的进展中起着重要作用。然而，lncRNA CCAT1 在结直肠癌中的作用尚不清楚。在本研究中，我们发现 lncRNA CCAT1 的水平在结直肠组织和细胞系中均升高。下调 lncRNA CCAT1 抑制结直肠细胞系的增殖、迁移和侵袭，并促进细胞凋亡。我们随后发现 hsa-miR-4679 可以直接与 lncRNA CCAT1 结合，通过进一步的功能分析，我们证实 lncRNA CCAT1 作为 hsa-miR-4679 的海绵体促进了结直肠癌的进展。接下来，我们发现 hsa-miR-4679 可以直接与 GNG10（鸟嘌呤核苷酸结合蛋白，γ 10）的 3'UTR 结合。GNG10 的过表达促进了结直肠癌的进展，而这种表型可以被 miR-4679 模拟物逆转。最后，我们敲低了 CCAT1，发现 sh-CCAT1 降低了肿瘤的大小和增殖细胞的数量。总之，我们的研究结果表明，lncRNA CCAT1 通过 hsa-miR-4679/GNG10 轴促进了结直肠癌的进展，并为结直肠癌提供了新的潜在治疗靶点。
