Novel therapeutic protocol in the research of breast cancer treatment - Targeting the border

The complex signaling pathways and interactions inside and among cells which are responsible for the appearance and evolving of malignancy have a distinct and well separated border, the translation process, where the signals of a mutant and dysregulating genome are becoming specific proteins evolving to the malignant phenotype. We selected as translation target the Fragile X–Mental Retardation Protein (FMRP) of the breast cancer cell, a protein of whose role in translation has not clearly elucidated yet. Triple negative breast cancer cell lines (BCCL)-(BT20, MDA-MB-231, Hs578 T) were transfected by plasmid with mutant FMRP at progressively increased CGG triplets (from 45 to 200 repeats at a one by one CGG repeat step up process) and the production of the mutant protein was verified with the SUNSET method and Western blot analysis. Afterwards, the impact in proteinosynthesis inhibition and apoptosis induction of the transfected BCCL in relation to normal epithelial breast cell lines (NEBCL) was evaluated. Preliminary in vitro results showed slower rates of proteinosynthesis and higher apoptotic rate of the 78 CGG & 84 CGG repeat mutant FMRP transfected BCCL in compared to NEBCL, while for all other transfected BCCL no statistically significant differentiation was found.