The motility of breast cancer cells is stimulated by HMGB1/RAGE interaction but the truncated form lacking the C terminus has no effect

HMGB1/RAGE is identified as a ligand-receptor pair that plays an important role in tumorogenesis. HMGB1 and RAGE levels are higher most human tumors their overexpression associated with tumor progression. The causes of breast cancer still poorly understood. One reason might be the existence subtypes within various cellular mechanisms hormone-dependent hormone -independent malignant processes. We investigated effect protein its truncated form lacking C terminus on expression cell motility lines; MCF7-noninvasive, MDA-MB-231-invasive normal epithelial one MCF10. results demonstrate effects HMGB1∆C through association observed exclusively for independent MDA-MB-231 line. mobility cells was stimulated only by full length HMGB1. Our suggest signaling should considered essential process development cancers great invasive potential. blocking molecule ”locks” receptor inactivates it. This makes tailless promising therapeutic agent competes biologically active ligand prevents downstream RAGE.