LncRNA TUG1通过miR-145/KIAA1199轴对结直肠癌细胞转移和上皮间质转化的影响

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Abstract Objective To investigate the effect of LncRNA TUG1 on colorectal cancer cell metastasis and epithelial mesenchymal transformation (EMT) through microRNA-145 (miR-145)/KIAA1199 axis. Methods A total of 30 patients with colorectal cancer who were pathologically confirmed and did not receive preoperative chemoradiotherapy were collected from the First Hospital of Jiaxing, Zhejiang Province from August 2020 to February 2021. Differential expressions of lncRNA TUG1, miR-145, and KIAA1199 in Colo320, HCT116, and NCM460 cells, cancer and paracancerous tissues were detected by RT-qPCR; the effect target and correlation of LncRNA TUG1 and miR-145 were analyzed; the effects of lncRNA TUG1 on Colo320 cell development and KIAA1199 expression via miR-145 were detected; the effects of TUG1 or KIAA1199 down-regulation on Colo320 cell proliferation, invasion, and EMT were detected. Results The expression levels of lncRNA TUG1 and KIAA1199 in cancer tissues were higher than those in paracancerous tissues, and the expression level of miR-145 was lower than that in paracancerous tissues (P < 0.01). The expression levels of LncRNA TUG1 and KIAA1199 in HCT116 and Colo320 cells were higher than those in NCM460 cell, and the expression level of miR-145 was lower than that in NCM460 cell (P < 0.01). The cell viability (24, 48, 72 h) and invasion number of TUG1 down-regulated group were lower than those of down-regulated control group (P < 0.05); the expression levels of N-cadherin, Vimentin, and Snail in TUG1 down-regulated group were lower than those in down-regulated control group, while the expression of E-cadherin was higher than that in down-regulated control group (P < 0.01). The lucifase activity of LncRNA TUG1 wildtype+miR-145 mimics group was lower than that of LncRNA TUG1 wildtype+ mimics control group (P < 0.01); there was no significant difference in lucifase activity between LncRNA TUG1 mutant+ mimic group and LncRNA TUG1 mutant+miR-145 mimic group (P > 0.05). The number of cell invasion and cell viability (24, 48, 72 h) in TUG1 overexpression+miR-145 mimics group were higher than those in overexpression control+miR-145 mimics group (P < 0.05); the expression levels of N-cadherin, Vimentin, and Snail in TUG1 overexpression+miR-145 mimics group were higher than those in overexpression control+miR-145 mimics group, while the expression level of E-cadherin was lower than that in overexpression control+miR-145 mimics group (P < 0.01). The cell viability (24, 48, 72 h) and invasion number of KIAA1199 down-regulated group were lower than those of down-regulated control group (P < 0.05); the expression levels of N-cadherin, Vimentin, and Snail in KIAA1199 down-regulated group were lower than those in down-regulated control group, while the expression level of E-cadherin was higher than that in down-regulated control group (P < 0.01). Conclusion LncRNA TUG1 promotes KIAA1199 expression through miR-145 and accelerates the proliferation, invasion, and EMT of Colo320 cell.

Key words： Long non-coding TUG1 microRNA-145 KIAA1199 Colorectal cancer

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	LI Haiqiang LI Yan SHEN Xuning JIANG Honggang

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LI Haiqiang LI Yan SHEN Xuning JIANG Honggang. Effect of lncRNA TUG1 on colorectal cancer cell metastasis and epithelial mesenchymal transformation through miR-145/KIAA1199 axis#br#[J]. 中国医药导报, 2021, 18(36): 8-13.

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https://www.yiyaodaobao.com.cn/EN/ OR https://www.yiyaodaobao.com.cn/EN/Y2021/V18/I36/8

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