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Background: Prostate cancer is the most common form of non-dermatologic cancer and the second leading
cause of cancer deaths in the United States. Survival rate for the advanced disease still remains low, so current research
is aimed at alternative or adjuvant treatments that will target components of the signal pathways in the progression of
carcinogenesis with little or no cytotoxicity. In this study we investigated the effect of genistein on expression levels of
genes involved in the immune response pathways. The mechanism of genistein-induced cell death was also investigated.
The chemosensitivity of the LNCaP prostate cancer cells to genistein was investigated using ATP and MTS assays, and a
caspase binding assay was used to determine apoptosis induction. Several molecular targets/genes were determined using
cDNA microarray and RT-PCR analysis.
Results: The overall data revealed that genistein induces cell death in a time- and dose-dependent manner, and regulates
expression levels of several genes involved in carcinogenesis and immunity including MHC genes that are involved in
immune recognition of cells and the DefB1 and the HLA membrane receptor genes involved in immunogenicity.
Conclusion: The results of the study indicate that genistein inhibits carcinogenesis of LNCaP prostate cancer growth
via regulation of the identified specific targets/pathways in immunogenicity/immune response. The results thus provide
significant insight into the roles that genistein could play in immune response to prostate cancer proliferation and potential
role in immunotherapy and/or adjuvant therapeutic regimen.