Fig. 8
From: Nuclear FAM289-Galectin-1 interaction controls FAM289-mediated tumor promotion in malignant glioma
Schematic representation of the proposed mechanism of FAM289 in GBM cells. FAM289 contributes to tumorigenesis in malignant glioma by interacting with Galectin-1 to promote FAM289 protein translocation into cell nucleus, which could activate the ERK pathway to up regulate DNMTs expression and increase stem-like property gene expression, thereby affecting its drug sensitivity of TMZ in the treatment of glioma. Gal-1: Galectin-1, β1: β1 integrin, p: phosphorylation