Cyclin E, HER-2 and p53, are considered as major prognostic markers in breast 
cancer. As they are related in patho-clinical level, we aimed to check if they 
have any direct interaction on expression of each other. To study the effect of 
cyclin E on HER-2 expression, cell lines stably overexpressing cyclin E or its 
low molecular weight (LMW) isoforms were generated. To understand the results of 
p53 silencing either alone or in combination with cyclin E overexpression, we 
created three different p53 stably knocked down cell lines. Protein expression 
was analyzed by western blot, HER-2 expression in the established cell lines 
were determined using SYBR green real time PCR and data analyzed by REST 
software. Results indicate that HER-2 expression is only downregulated following 
p53 silencing and none of cyclin E isoforms can alter its expression. The 
presence of cyclin E isoforms in p53 silenced clones also does not altered HER-2 
expression. Given the fact that p53 degradation is increased by HER-2 
overexpression, these data can draw a regulatory loop in which a non-mutated 
functional p53 and HER-2 can bidirectionally regulate the expression of these 
two genes. This study improves our understandings of these pathways and these 
proteins can be introduced either as a marker or as a target in cancer 
treatment.