Mechanism of Glucose Transporter Protein 1 Mediating Malignant Behavior in Breast Cancer Through the PI3K/Akt Signaling Pathway

Abstract

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.