Abstract: Objective　To study the effect of long non-coding RNA (lncRNA) FOXC1 promoter upstream transcript (FOXCUT) on the proliferation and invasion of colon cancer cell (HCT116) and its mechanism. Methods　 HCT116 cells transfected with FOXCUT siRNA were used as FOXCUT siRNA group. The transfection-negative interfering RNA was used as the negative control group (FOXCUT siRNA-NC group), and the untransfected group was used as the normal control group (NC group). The qPCR method was used to determine the FOXCUT interference effect and to detect the mRNA expression levels of FOXCUT in colon cancer and adjacent tissues, human colon cancer (SW480, SW620, HCT116, HT29) and human normal colon epithelial cells (NCM460). The effects of silencing FOXCUT on the proliferation and the invasion of HCT116 cells were detected by Cell Counting Kit-8 (CCK-8), colony forming assay and Transwell assay. qPCR was used to detect the mRNA expressions of Notch1 and Hes1 in HCT116 cells after FOXCUT silencing, and Western blot assay was used to detect the protein expressions of Notch1 and Hes1 in HCT116 cells. Results　Compared with adjacent tissues, the expression level of FOXCUT mRNA increased significantly in colon cancer tissues (P＜0.01). Compared with NCM460 cells, the FOXCUT mRNA expression levels increased significantly in colon cancer cell lines SW480, SW620, HCT116, and HT29 (P＜0.05), and the expression level was the highest in HCT116 cells. Compared with the FOXCUT siRNA-NC group, the FOXCUT mRNA expression levels were significantly reduced in HCT116 cells of the FOXCUT siRNA group (P＜0.01). There was no significant difference in the FOXCUT mRNA expression level in the HCT116 cells between the NC group and FOXCUT siRNA-NC group (P＞0.05). The silencing FOXCUT could significantly inhibit the proliferation and invasion of HCT116 cells (P＜0.05), and inhibit the mRNA and protein expressions of Notch1 and Hes1 in HCT116 cells (P＜0.01). Conclusion　Silencing FOXCUT can inhibit the proliferation and invasion of HCT116 cells, which may be related to the inhibition of Notch pathway.

Key words: RNA, long noncoding, colonic neoplasms, HCT116 cells, cell proliferation, neoplasm invasiveness, receptor, Notch1, transcription factor HES-1