葡萄糖转运蛋白1通过PI3K/Akt信号通路介导乳腺癌恶性行为的机制

IF 0.9 4区 材料科学
Kai Lin, Xinghua Wu, Yuying Qi, Kaiyin Wang, Yunzhu Guan, Tinghui Hu
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引用次数: 0

摘要

探讨GLUT1通过PI3K/Akt信号通路介导乳腺癌发展的作用机制。通过添加IGF-1 (PI3K/AKT信号通路的激活剂)的siRNA实现了乳腺癌细胞系MDA-MB-231 GLUT1的敲低。实验组为NC、shGLUT1、shNC+IGF-1、shGLUT1+IGF-1。采用MTT、Transwell和划痕修复法观察乳腺癌细胞的增殖、侵袭和迁移行为;Western blot检测PI3K-AKT信号通路中p-PI3K、p-AKT、p-mTOR蛋白表达水平。敲除GLUT1后,PI3K/AKT信号通路关键蛋白p-PI3K、p-AKT、p-mTOR的表达水平显著降低。单独加入IGF-1后,p-PI3K、p-AKT、p-mTOR蛋白表达水平下降趋势更为明显,癌细胞的增殖、侵袭等细胞功能也均受到抑制。GLUT1可通过PI3K/Akt信号通路促进乳腺癌的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanism of Glucose Transporter Protein 1 Mediating Malignant Behavior in Breast Cancer Through the PI3K/Akt Signaling Pathway
To investigate the mechanism of action of GLUT1 in mediating breast cancer development through the PI3K/Akt signaling pathway. Knockdown of breast cancer cell line MDA-MB-231 GLUT1 was achieved by siRNA with the addition of IGF-1, an activator of the PI3K/AKT signaling pathway. The experimental groupings were NC, shGLUT1, shNC+IGF-1, and shGLUT1+IGF-1. The proliferation, invasion, and migration behaviors of breast cancer cells were observed by MTT, Transwell, and scratch-repair assays; Western blot was used to detect the protein expression levels of p-PI3K, p-AKT, and p-mTOR in the PI3K-AKT signaling pathway. After the knockdown of GLUT1, the expression levels of key proteins of the PI3K/AKT signaling pathway, p-PI3K, p-AKT, and p-mTOR, were significantly decreased. After the addition of IGF-1 alone, the decreasing trend of the protein expression levels of p-PI3K, p-AKT, and p-mTOR was even more pronounced, and the cellular functions of the cancer cells, such as proliferation and invasion, were also all inhibited. GLUT1 can promote breast cancer development through the PI3K/Akt signaling pathway.
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来源期刊
Science of Advanced Materials
Science of Advanced Materials NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
11.10%
发文量
98
审稿时长
4.4 months
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