RAP1GDS1在儿茶素抑制舌鳞癌细胞Glut1表达中的作用

IF 0.1 4区 医学
W. Su, Pan Liu, Yang Zhang, Zhongcheng Gong, Hua-rong Zhao
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摘要

背景:本研究旨在探讨Glut1在儿茶素抑制舌鳞癌细胞侵袭和迁移能力中的作用。材料和方法:采用Transwell法和划痕法测定儿茶素对细胞侵袭和迁移的影响,WB法检测各蛋白的表达。过度表达的慢病毒被用来上调舌鳞状细胞中的Glut1,以检测这一过程是否可以逆转。通过RNAi技术沉默舌鳞癌细胞中的RAP1GDS1后,测量儿茶素对Glut1表达的影响。结果:Transwell试验和划痕试验结果证实儿茶素具有抑制入侵和迁移的作用。随后的WB实验证实,儿茶素可以抑制Glut1、N-钙粘蛋白和波形蛋白的表达,同时促进E-钙粘蛋白的表达。Glut1的上调可以显著逆转儿茶素的抑制作用。RAP1GDS1的沉默可抑制Glut1的表达。然而,Glut1表达的上调可以显著逆转这一过程。WB结果证实儿茶素对舌鳞癌细胞RAP1GDS1的抑制作用。结论:儿茶素通过下调Glut1影响糖酵解活性,并诱导EMT过程抑制。推测通过沉默RAP1GDS1。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of RAP1GDS1 in the Inhibition of Glut1 Expression by Catechins in Tongue Squamous Carcinoma Cells
Background: The paper aimed to investigate the role of Glut1 in the inhibition of the invasion and migration capabilities of tongue squamous carcinoma cell by Catechin. Materials and Methods: Transwell assay and scratch test were applied to measure the effect of Catechin on the invasion and migration of the cells, and WB to detect the expression of each protein. Overexpressed lentivirus was used to up-regulate Glut1 in tongue squamous carcinoma cells, detecting whether the process can be reversed. After silencing RAP1GDS1 in tongue squamous carcinoma cells by RNAi technology, the effect of Catechin on Glut1 expression was measured. Results: The results of Transwell assay and scratch test verified that Catechin can inhibit the invasion and migration. Subsequent WB experiments confirmed that Catechin can inhibit the expression of Glut1, N-cadherin and Vimentin, while promote the expression of E-cadherin. The up-regulation of Glut1 can significantly reverse the inhibitory effect of Catechin. Silencing of RAP1GDS1 can inhibit the expression of Glut1. However, the up-regulation of Glut1 expression can significantly reverse this process. WB result verified the inhibitive effect of Catechin on RAP1GDS1 in tongue squamous carcinoma cells. Conclusion: Catechin affects glycolytic activity by down-regulating Glut1 and induces EMT process inhibition. It is speculated that, through regulating Glut1 by silencing RAP1GDS1.
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