S Chen1, H Yuan, B-C Chen, Z-A Wan, S-L Tu, X-Y Hu. 1. Department of Colorectal Surgery, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China. hxy16848@163.com.
Abstract
OBJECTIVE: To detect the expression level of long intergenic non-protein coding RNA 1198 (LINC01198) in colorectal cancer (CRC) tissues and cells, to investigate the effect of LINC01198 on the biological function of CRC cells through in vivo and in vitro experiments, and to explore its molecular mechanism. PATIENTS AND METHODS: Tissue samples were collected from 32 patients with CRC. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect the relative expression level of LINC01198 in CRC tissues and cells. In vitro experiments [Cell Counting Kit-8 (CCK-8) and flow cytometry] were conducted to explore the effect of interfering with the expression of LINC01198 on the proliferation, cycle and apoptosis of CRC cells. Tumorigenesis assay was undertaken in nude mice to investigate the influence of LINC01198 on the tumorigenic ability of CRC cells in vivo. Besides, Western blotting was performed to determine the changes in the downstream signaling pathway of LINC01198. RESULTS: Among the 32 cases of tissue samples of CRC patients, 28 cases had an upregulated expression of LINC01198 compared with paracancerous tissues. The results of qRT-PCR indicated that LINC01198 expression was upregulated in CRC cells, and the interference efficiency of si-LINC01198 was measured via qRT-PCR. The results of in vitro experiments demonstrated that after interfering with the expression of LINC01198 in CRC cells, cell proliferation capacity was inhibited, cell cycle was arrested at G1/G0 phase, and the apoptosis rate was increased. The results of nude mice tumorigenesis experiments revealed that after interfering with the expression of LINC01198, the tumorigenic ability of CRC cells in vivo declined. Additionally, Western blotting assay results confirmed that after interfering with the expression of LINC01198, the expression of molecular markers in the Notch signaling pathway was inhibited. CONCLUSIONS: The expression of LINC01198 is upregulated in the case of CRC, which promotes proliferation and inhibits apoptosis of CRC cells by regulating the Notch signaling pathway. Our findings provide a novel biomarker for the diagnosis and treatment of HCC patients and treatment strategies.
OBJECTIVE: To detect the expression level of long intergenic non-protein coding RNA 1198 (LINC01198) in colorectal cancer (CRC) tissues and cells, to investigate the effect of LINC01198 on the biological function of CRC cells through in vivo and in vitro experiments, and to explore its molecular mechanism. PATIENTS AND METHODS: Tissue samples were collected from 32 patients with CRC. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect the relative expression level of LINC01198 in CRC tissues and cells. In vitro experiments [Cell Counting Kit-8 (CCK-8) and flow cytometry] were conducted to explore the effect of interfering with the expression of LINC01198 on the proliferation, cycle and apoptosis of CRC cells. Tumorigenesis assay was undertaken in nude mice to investigate the influence of LINC01198 on the tumorigenic ability of CRC cells in vivo. Besides, Western blotting was performed to determine the changes in the downstream signaling pathway of LINC01198. RESULTS: Among the 32 cases of tissue samples of CRC patients, 28 cases had an upregulated expression of LINC01198 compared with paracancerous tissues. The results of qRT-PCR indicated that LINC01198 expression was upregulated in CRC cells, and the interference efficiency of si-LINC01198 was measured via qRT-PCR. The results of in vitro experiments demonstrated that after interfering with the expression of LINC01198 in CRC cells, cell proliferation capacity was inhibited, cell cycle was arrested at G1/G0 phase, and the apoptosis rate was increased. The results of nude mice tumorigenesis experiments revealed that after interfering with the expression of LINC01198, the tumorigenic ability of CRC cells in vivo declined. Additionally, Western blotting assay results confirmed that after interfering with the expression of LINC01198, the expression of molecular markers in the Notch signaling pathway was inhibited. CONCLUSIONS: The expression of LINC01198 is upregulated in the case of CRC, which promotes proliferation and inhibits apoptosis of CRC cells by regulating the Notch signaling pathway. Our findings provide a novel biomarker for the diagnosis and treatment of HCC patients and treatment strategies.