The effect of p-4E-BP1 and p-eIF4E on cell proliferation in a breast cancer model.

摘要: Cell signaling pathways and protein translation are crucial for understanding malignant transformation. 4E-BP1 the eIF4F complex regulate cap-dependent translation. We investigated how eIF4E phosphorylation status affects in vitro vivo cell proliferation a breast cancer model. Cells from 2 carcinoma lines (MDA-MB 231 MDA-MB 468) human fibroblasts (IMR90 cells) were infected with retrovirus carrying wild-type or mutant unable to hyperphosphorylate. Overexpression of induced significant decrease IMR90 468 cells, but not cells. A correlation was observed between baseline-phosphorylated (p-eIF4E) levels sensitivity transduction. By co-immunoprecipitation, p-eIF4E seemed present lower affinity than total After treatment CGP57380, MAP kinase-interacting kinase (MNK) inhibitor, downregulation associated an increase E-cadherin β-catenin expression. These results provide evidence that transduction leads proliferation, high may counteract suppressor effect 4E-BP1. propose p-4E-BP1 central factors reflect oncogenic potential cancer.