Journal: Cellular and molecular life sciences : CMLS
Article Title: RIP140 inhibits glycolysis-dependent proliferation of breast cancer cells by regulating GLUT3 expression through transcriptional crosstalk between hypoxia induced factor and p53.
doi: 10.1007/s00018-022-04277-3
Figure Lengend Snippet: Fig. 7 Model describing how RIP140 inhibits tumorigenesis by affecting glycolysis through the blockade of GLUT3 expres- sion. RIP140 and p53 cooper- ate to inhibit the expression of GLUT3 induced by HIF-α. Glycolysis-dependent prolif- eration of breast cancer cells is reduced, due to a decrease in glycolysis. The prognostic value of RIP140 is associated with good survival in patients with low GLUT3, high p53 and low HIF-α (left panel). In patients with high HIF-α, low p53 and high GLUT3, RIP140 and p53 do not inhibit the tran- scriptional activity of HIF-α; GLUT3 is highly expressed and glycolysis is enhanced. In this sub-group, RIP140 expression level is not correlated with good survival (right panel). Double thick blue lines represent cyto- plasmic membranes, double thin ones that of nucleus. The grey square represents GLUT3 gene, the grey ovoid forms represent GLUT3 protein. The orange circle represents glucose.
Article Snippet: Immortalized MEF#1 were transduced with lentiviral particles expressing shRNA against murine GLUT3 (sc41219-V) according to the manufacturer’s protocol (Santa Cruz Biotechnology, Dallas, USA).
Techniques: Expressing, Activity Assay