Bachground 
Prostate cancer (PCa) is one of the main causes of death and morbidity among men worldwide. CEMIP (cell migration-inducing hyaluronidase) is found at high levels in various cancers. High CEMIP levels are associated with cancer progression making it an important molecular marker for metastasis and a potential therapeutic target for treatments aimed at controlling metastasis. The role in cancer of 11-zinc finger protein (CTCF), renown transcription factors, is complex since it can act as tumor suppressor or be a driver of cancer. Role of CTCF in genome organization could influence the expression of CEMIP , although this specific interaction is not fully detailed.

Objective
To investigate the epigenetic and transcriptional role of 11-zinc finger protein (CTCF) on CEMIP that drives its metastatic phenotypes in aggressive prostate cancer and Novel and translational target for drug resistant prostate cancer

Methods
ChIP-Atlas and UCSC Genome Browser were used as a tool to examine CTCF and its binding site with CEMIP. CEMIP was knock-downed (si-RNA) and overexpressed (OE) with lentivirus in androgen-insensitive (DU145, PC-3) and androgen-sensitive (LNCaP) human prostate cancer cell lines. We then performed 3D spheroid model (Aggrewell method) to furtherly confirm that the knock-down and overexpression of CEMIP play crucial role in 3D spheroid formation in castration-resistant prostate cancer cell lines with statistical analysis from GraphPadPrism software.
Results
The results revealed the significant epigenetic shift of CEMIP at promoter region affected by CTCF. The results from RT-qPCR confirmed the successful knock-down and overexpression. The knock-down displayed cytotoxic effects against cancer cells (p < 0.05) while the overexpression of CEMIP increased cancer cells proliferation (p < 0.05). Moreover, cancer cells form less aggregation after si-CEMIP but better 3D structure in OE. Thus, we confirmed that CEMIP drives tumor metastasis and 3D spheroid formation in castration-resistant prostate cancer cell lines
Conclusion
Our investigations provide compelling and novel evidence that CEMIP has role as biomarkers in androgen-resistant prostate cancer. Overall, our outcomes reveal that CEMIP may have potential as a future therapeutic target in prostate cancer.