Small molecules targeting ULK1 in triple-negative breast cancer treatment

With a low survival rate, triple-negative breast cancer (TNBC) is a disease difficult to treat and is mainly confined to females. Traditional therapies have bad effects on slowing down the spread of this kind of cancer, so it is essential and urgent to look for a newly developed treatment for TNBC. Defective autophagy is implicated in tumorigenesis, both as a tumor inhibitor preventing the accumulation of damaged proteins and organelles and as a cell survival mechanism that can promote the growth of established tumors. Although autophagy is carried out by the synergistic action of more than 30 proteins, only a few of them are enzymes with clear drug-targeting potential. In addition, according to past studies, the absence of ULK1 alone is sufficient to eliminate autophagy in many cell types, highlighting its particularly important role. Based on a review of the previous work, this paper focuses on ULK1-controlled autophagy as a potential method of slowing down the spread of TNBC cells or even curing cancer and describes some molecules targeting ULK1.