An increase in MMP-2 and MMP-9 is associated with tumour progression but how the constitutive expression of these genes is regulated in prostate cancer is at present uncertain.
Because TMPRSS2 is regulated in the prostate by androgens, it was proposed that this gene rearrangement could be a mechanism whereby the ETV1 or ERG oncogenes were overexpressed, leading to prostate cancer.
Given the increase in intraprostatic adipocytes after TZD treatment, it was unclear whether these changes were regulated in adipocytes or prostate.
It is important to note that HOXD3 is expressed at detectable levels in normal prostate [43], as many homeobox genes are regulated in a spatial and temporal manner.
Collagen genes were also reported to be regulated by Se-methylselenocysteine in a prostate cancer cell line (LNCaP), but only one of these (Col4a5) was regulated in the same direction in the present study [ 17].
Notably, in clinical prostate samples, androgenic control of the expression of CXCR4 and CXCR7 is regulated in reciprocal fashion.
Ambac is regulated in Wisconsin.
In these studies, miR-520c was down regulated in prostate cancer tissues and it was suggested that it is involved in tumor migration and invasion, thus constituting a metastasis-promoting miRNA [ 33].
It is likely that one or more of these proteins are differentially regulated in prostate cancer and as a result increase the threshold required for Fas receptor activation and apoptosis following engagement of Fas receptor with Fas ligand.
In particular, CUL3, over expressed in kidney and prostate cancers, is a target of several dysregulated MIRs: MIR22, MIR23A, MIR23B, MIR218-1, MIR218-2, and MIR301, which are down regulated in kidney cancers, and of MIR22, MIR23A, MIR181A, and MIR181C, which are down regulated in prostate cancers (Table 5).
