Prostate tumor-inducing gene

Recently, it has been found that, in addition to its detoxification function and its function as a biomarker for up-regulation of other phase II enzymes, up-regulation of quinone reductase by monofunctional inducers may play a role in the stabilization of p53, the protein product of a tumor suppressor gene, which induces growth arrest and apoptosis. Sulforaphane has also been shown to mediate growth arrest and induce cell cycle arrest and apoptosis in many cancer cell lines, including those of human prostate, colon, and T-cell leukemia origin. - The exact mechanisms, and whether all the bioactivities of sulforaphane involve the ARE, are not yet understood. 

COX-2 overexpression also has been detected in prostate adenocarcinoma (Gupta et al, 2000 Yoshimura et al, 2000). The expression of COX-2 in tumors, was found to be upregulated by various oncogenes such as Her-2 or ras and downregulated by tumor suppressor genes like p53 (Subbaramaiah et al., 1999 Subbaramaiah et al, 2002). Several COX-2 inhibitors such as celecoxib and NS-398, have been demonstrated to induce apoptosis in prostate cancer cell lines (Hsu et al., 2000 Liu et al., 1998). 

Majid S, Dar AA, Shahryani V, Hirata H, Ahmad A, Saini S, Tanaka Y, Dahiya AV, Dahiya R. Genistein reverses hypermethylation and induces active histone modifications in tumor suppressor gene B-cell translocation gene 3 in prostate cancca-. Cancer. 2010 116 66-76. 

Olson, M.V., Lee, J., Zhang, E, Wang, A., and Dong, Z. (2006). Inducible nitric oxide synthase activity is essential for inhibition of prostatic tumor growth by interferon-beta gene therapy. Cancer Gene Ther. 13, 676-685. 

Recently, Mu et al. (2003) have reported that the KCNK9 potassium channel (TASK) gene is amplified and overexpressed in breast cancers, lung and prostate cancers. Moreover, overexpression of KCNK9 was found in 57 (46.0%) of the 124 patients with colorectal carcinomas, but not in the patients with colorectal adenoma (Kim et al. 2004). Interestingly, overexpression of KCNK9 promotes tumor formation and induces resistance to both hypoxia and serum deprivation. 

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