Abstract
Limited therapeutic options impede the clinical outcome of triple-negative breast cancer (TNBC). Our recent study uncovered a novel signaling pathway implicating gamma-butyrobetaine hydroxylase 1 (BBOX1) in the control of cell growth in TNBC, via inositol 1, 4, 5-trisphosphate receptor type 3 (IP3R3) mediated calcium signaling which is essential for cellular energy metabolism.