Breast cancer is one of the most common cancers in women and it is highly treatable by radiotherapy and/or radiochemotherapy. A global analysis of the protein expression pattern was performed to identify radiation-responsive proteins in MCF-7 breast cancer cells using 2D-PAGE coupled with MALDI-TOF-MS. When MCF-7 cells were exposed to ionizing radiation (IR) such as γ-rays, eight proteins (GH2, RGS17, BAK1, CCNH, TSG6, RAD51B, IGFBP1, and CASP14) were up-regulated and three proteins (C1QRF,

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... R2, and p34 SE1-1 ) were down-regulated. In an effort to find what mechanisms are responsible for these changes, we initially focused on p34 SE1-1 , which is known as a transcriptional regulator and oncogene. Our results show that p34 SE1-1 expression is significantly decreased only at the protein level but not at the transcriptional level after IR treatment. We suggest that the B55 regulatory subunit of PP2A, a positive regulator of p34 SE1-1 , is at least partly responsible for the decreased p34 SE1-1 expression, in which the B55 regulatory subunit of PP2A was down-regulated at the protein level as a cellular response to IR. We, therefore, propose that inactivated PP2A resulting from the absence of the B55 subunit may not be able to dephosphorylate p34 SE1-1 and therefore increase the phosphorylated form of p34 SE1-1 with low stability. Our further extended study shows that the p34 SE1-1 expression level was not changed after H 2 O 2 treatment at either protein or transcriptional levels. This result implies that MCF-7 cells seem to use different signaling pathways in response to IR and H 2 O 2 stresses although both of them belong to the same DNA damage inducing stimuli of reactive oxygen species (ROS).