
-   There are two p53 DNA-binding sites located in the Cathepsin D (CD)-promoter which appear to mediate transactivation of a CD-promoter luciferase-reporter during p53-dependent apoptosis. The findings suggest that these observations link CD protease to p53-dependent tumor suppression and chemosensitivity [PMID: 9619826].
-   In human breast cancer cells, cathepsin-D and pS2 mRNAs are specifically and directly induced by estrogens at the transcriptional level, and pS2 mRNA, like cathepsin-D mRNA, are rapidly induced by epidermal growth factor [PMID: 2612733]. Peptide growth factors, such as insulin, insulin-like growth factor I, and basic fibroblast growth factor, can also increase the steady state levels of cathepsin-D and pS2 mRNAs in breast cancer cell lines. Overall, cathepsin-D and pS2 genes are under complex regulation in breast cancer cells, since growth factors stimulate their expression via indirect mechanisms contrasting with the primary transcriptional effects of estrogens [PMID: 2664475].
-   RhoA and RhoC play different, but clear, roles in ERalpha signaling by similarly modulated ERalpha recruitment to the vitellogenin estrogen responsive element (ERE) present in a luciferase reporter gene and to the promoters of progesterone receptor (PR), cathepsin D, and pS2 genes. RhoA up-regulated the ERE-luciferase reporter gene activity and PR mRNA expression and tended to down-regulate cathepsin D and pS2 mRNA expression. These GTPases are definitely involved, along with RhoB, in ERalpha recruitment and, to some extent, ERalpha cofactor balance [PMID: 24096540].
