A more reliable approach may be to assess the level of transcription in cancer samples. In our study, we attempted to measure transcription. As an electron donor, Trx is essential to cellular function of Prx [17]. Of the two isoforms of human Trx, cytoplasmic Trx1 and mitochondrial Trx2, we focused on Trx1 in breast cancer tissue because of its localization with Prx I. As with Prx I, there are many
reports that Trx1 may be closely associated buy GANT61 with cancers. Previous studies have shown the expression of Trx1 in a number of human cancer tissues [26–28, 33, 34]. Estrogen receptors and p53 are important transcription factors in the growth regulation of cancer cells in breast RNA Synthesis inhibitor cancer. Previous findings suggest that Trx1 expression is linked to the estrogen receptor-dependent and p53-dependent regulation of growth in breast cancer cells [34]. This observation is consistent with the association
of Trx1 and breast cancer. In the present study, we demonstrated that increasing Trx1 expression was associated with progress of breast cancer, and that Trx1 was correlated with Prx I in human breast cancer. It is not certain that, in breast cancer, the involvement of Trx1 reflects its ability to regulate Prx I action, but at least in terms of magnitude of expression in the same patients, the Sepantronium cost association of Trx1 with Prx1 supports the theory that their functions are related to each other in breast cancer. Conclusion We have demonstrated here that Prx I and Trx1 are preferentially overexpressed in human breast carcinoma and the expression levels are associated
with tumor grade. In addition, Prx I expression is correlated with Trx1 expression in breast cancer. We found that mRNA levels for both Prx I and Trx1 in normal breast tissue are extremely low compared with those of many other major human tissues. Based on these observations, we suggest that Prx I and Trx1 could be used as potential breast cancer markers. Acknowledgements This work was financially supported by Regional Research and Development Cluster Project (B0009735) funded by the Ministry of Knowledge Economy (MKE) of Korea. References 1. Sundaresan M, Yu ZX, Ferrans VJ, Irani K, Finkel T: Requirement for generation of H 2 O 2 for platelet-derived growth factor signal transduction. Science 1995, 270: 296–299.CrossRefPubMed 2. Finkel T: Oxygen radicals and signaling. Curr Opin Cell Biol 1998, 10: 248–253.CrossRefPubMed 3. Kang SW, Chae HZ, Seo MS, Kim K, Baines IC, Rhee SG: Mammalian peroxiredoxin isoforms can reduce hydrogen peroxide generated in response to growth factors and tumor necrosis factor-alpha. J Biol Chem. 1998, 273 (11) : 6297–6302.CrossRefPubMed 4.