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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Nuclear FAM289-Galectin-1 interaction controls FAM289-mediated tumor promotion in malignant glioma

Fig. 4

FAM289 and Galectin-1 interdependently regulate tumor proliferation and migration via ERK and NF-kB signaling pathways. (A) FAM289 upregulation increased p-ERK and p-NF-kB expression in U251 cells. (B) FAM289 decreased p-ERK and p-NF-kB expression in U87-MG cells. (C&D) Screening of more than 40 genes downstream of ERK and NF-kB by qPCR and western blotting. The expressions of DNMT1and DNMT3B were regulated by FAM289 in U251 and U87-MG cells. (E) Protein levels of p-ERK, p- NF-kB, DNMT1 and DNMT3B in Galectin-1 siRNA1- and control siRNA-transfected U251 con or U251-FAM289OE cells were detected by western blotting. (F) Protein levels of p-ERK, p- NF-kB, DNMT1and DNMT3B in Galectin-1-flag- and control plasmid-transfected U87-MG con or U87-MG-FAM289KD cells were detected by western blotting. (G&H) The effects of MAPK and NF-kB inhibitors on FAM289-induced expression of DNMT1 and DNMT3B. U251 and U87-MG cells were treated with or without U0126 (U, 1 μM), PDTC (SP, 1 μM) for 24 h and subjected to western blot analysis. n = 3, *p < 0.05, * *p < 0.01 vs. Control (−)

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