The transcription factor gene MYC is important in breast cancer, and its mRNA is 
maintained at a high level even in the absence of gene amplification. The 
mechanism(s) underlying increased MYC mRNA expression is unknown. Here, we 
demonstrate that MYC mRNA was stabilized upon estrogen stimulation of estrogen 
receptor-positive breast cancer cells via SRC-dependent effects on a recently 
described RNA-binding protein, IMP1 with an N-terminal deletion (ΔN-IMP1). We 
also show that loss of the tumor suppressor p53 increased MYC mRNA levels even 
in the absence of estrogen stimulation. However, in cells with wild-type p53, 
SRC acted to overcome p53-mediated inhibition of estrogen-stimulated cell cycle 
entry and progression. SRC thus promotes cell proliferation in two ways: by 
stabilizing MYC mRNA and by inhibiting p53 function. Since estrogen 
receptor-positive breast cancers typically express wild-type p53, these studies 
establish a rationale for p53 status to be predictive for effective SRC 
inhibitor treatment in this subtype of breast cancer.