SLC16A2基因缺失对U2OS骨肉瘤细胞的EMT过程的调节作用

Journal: Basic Medical Theory Research DOI: 10.12238/bmtr.v8i1.18548

刘松, 金宇

承德医学院附属医院

Abstract

目的:本研究旨在探讨SLC16A2基因在U2OS骨肉瘤细胞上皮-间充质转化(EMT)过程中的作用。方法:通过转染技术敲低U2OS细胞中SLC16A2基因,构建SLC16A2缺失的U2OS细胞模型,进一步通过实时荧光定量PCR分析EMT相关标志物mRNA的表达。结果:qPCR结果显示,SLC16A2在U2OS细胞中敲低成功;与对照组相比,EMT相关标志物mRNA表达发生显著变化,提示SLC16A2参与调控U2OS细胞EMT过程。结论:SLC16A2基因通过调控EMT通路中的关键分子,进而降低U2OS骨肉瘤细胞的转移能力。

Keywords

SLC16A2基因;骨肉瘤;上皮-间充质转化(EMT)

References

[1] Bi B,Tang L,Liang R,et al.MCT8 modulates metabolite uptake and T cell exhaustion to promote immunosuppression and tumor progression in hepatocellular carcinoma[J].Mol Can
[2] Prusinkiewicz MA,Gameiro SF,Ghasemi F,et al. Survival-
[3] Yang J,Weinberg RA.Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis[J]. Dev Cell,2008,14(6):818-829.
[4] Issagholian L, Tabaie E, Reddy AJ, et al. Expression of E-cadherin and N-cadherin in Epithelial-to-Mesenchymal Tra
[5] Sohrabi E,Moslemi M,Rezaie E,et al.The tissue expressi
[6] Li J, Xie J, Wu D, et al. A pan-cancer analysis revealed the role of the SLC16 family in cancer [J]. Channels (Austin), 2021,15(1):528-540.

Copyright © 2026 刘松, 金宇

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License