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We and others have recently shown that Id4 is highly expressed in the normal prostate and decreased in prostate cancer due to promoter hypermethylation .
Id4 expression in the prostate thus appears in contrast with the expression of other Id genes (Id1 and Id3) which are expressed at low to negligible levels in the normal prostate although their expression increases significantly in prostate cancer .
Our results suggest that loss of Id4 attenuates normal prostate development and promotes hyperplasia/dysplasia with subtle m PIN like lesions characterized by gain of Myc and Id1 and loss of Nkx3.1 and Pten expression.These results suggest that Id4 could potentially act within the androgen receptor pathway to regulate the development and function of the prostate.We used the Id4 -/- mouse model to evaluate further the role of Id4 in prostate development and its significance in prostate cancer.Decreased NKX3.1 expression was in part due to decreased androgen receptor binding on NKX3.1 promoter in Id4-/- mice.The increase in the expression of Myc, Sox9, Id1, Ki67 and decrease in the expression of PTEN, Akt and phospho-AKT was associated with subtle m PIN like lesions in Id4-/- prostates.
One of the mechanisms by which Id4 may regulate normal prostate development is through regulating androgen receptor binding to respective response elements such as those on NKX3.1 promoter.