The scope of the present review is to describe the advances in our understanding of the molecular basis of FUBP1 functions in normal cells and carcinogenesis.
ICA inhibited the expression of fuse binding protein 1 (FBP1), a critical regulator of proliferation and tumorigenesis through binding to the c‑Myc promoter, as well as β‑catenin, a key regulator in ovarian cancer initiation, metastasis, chemoresistance and recurrence.
Reinforcing LSD1+8a expression in FUBP1-downregulated neural progenitors restored terminal differentiation and suppressed tumorigenesis; hence, LSD1+8a is an obligatory effector of FUBP1-dependent neuronal differentiation.