A recent paper:  Loss of Nkx3.1 leads to the activation of discrete downstream target genes during prostate tumorigenesis.

Oncogene. 2009 Sep 17;28(37):3307-19. Epub 2009 Jul 13 [PubMed]
Song H, Zhang B, Watson MA, Humphrey PA, Lim H, Milbrandt J.

Song et al. have shown that loss of the androgen-regulated transcriptional regulator NKX3.1 leads to over-expression of a series of genes in a mouse model of prostate adenocarcinoma.  QSOX1 is one such gene and is highly expressed in the early stages of prostate tumorigenesis.

Song et al. write:

“Interestingly, quiescin Q6 expression is very high in early lesions, such as PIN, suggesting that this provides a selective advantage to cells in these early prostate cancer precursor lesions.”  [PIN: prostatic intraepithelial neoplasia]

and:

“Our in vitro experiments showed that quiescin Q6 is a direct target of the transcriptional repressor NKX3.1, suggesting that the increased levels of this pro-oxidant enzyme after loss of Nkx3.1 could mediate prostate tumor initiation through increased reactive oxygen species accumulation and subsequent oxidative damage, a tumorigenic influence in many cancers …”

Earlier precedent for the involvement of QSOX1 in prostate cancer comes from a 2005 study by Abate-Shen and colleagues.

Loss-of-function of Nkx3.1 promotes increased oxidative damage in prostate carcinogenesis.

Cancer Res. 2005 Aug 1;65(15):6773-9. [PubMed]
Ouyang X, DeWeese TL, Nelson WG, Abate-Shen C.

Ouyang et al. demonstrated that Nkx3.1 mutant mice showed very strong up-regulation of QSOX1 during the conversion of normal prostate epithelium to prostatic intraepithelial neoplasia (PIN).  They interpreted these results as one component of the disregulation of the cellular response to oxidative stress during prostate carcinogenesis.