Abstract
Abnormal genome hypermethylation participates in the tumorigenesis and development of prostate cancer. Prostate cancer cells highly express DNA methyltransferase 3 (DMNT3) family genes, essential for maintaining genome methylation. In the present study, multi-target siRNA, based on the homologous region of the DNMT3 family, was designed for the in vitro investigation of its effects on the proliferation, migration, and invasion of TSU-PR1 prostate cancer cells. The consequential cell-cycle derangement, through DNMT3A/B or only DNMT3B silencing, was partially efficient, without affecting apoptosis. DNMT3A silencing had absolutely no effect on changing TSU-PR1 cell biological behavior. Hence, DNMT3B alone apparently plays a key role in maintaining the unfavorable behavior of prostate-cancer cells, thereby implying its potential significance as a promising therapeutic target, with DNMT3A simply in the role of helper.
Highlights
Prostate cancer is the most common solid tumors in men in developed countries
Abnormal genome hypermethylation in the tumorigenesis and development of prostate cancer, with higher expression of DNMT proteins compared to normal prostate tissue, has been established (Benbrahim-Tallaa et al, 2007; Morey Kinney et al, 2008; Lin et al, 2011)
Hypermethylation of certain genes is very common in human cancers, including prostate cancer (Kim et al, 2010; Figure 3 - Results from proliferation (A), migration (B) and invasion (C, D) assays of TSU-PR1 cells after small interfering RNA (siRNA) transfection
Summary
Prostate cancer is the most common solid tumors in men in developed countries. Abnormal regulation of the enzymes involved in DNA methylation, and incorrect methylation of CpG islands, are all common phenomena in human tumors (Sharma et al, 2010). Abnormal genome hypermethylation in the tumorigenesis and development of prostate cancer, with higher expression of DNMT proteins compared to normal prostate tissue, has been established (Benbrahim-Tallaa et al, 2007; Morey Kinney et al, 2008; Lin et al, 2011). The DNMT3 subfamily includes DNMT3A and DNMT3B, crucial in the process of de novo genome methylation (Das and Singal, 2004; Siedlecki and Zielenkiewicz, 2006; Patra et al, 2008). The catalytic domain of DNMT3 resides in its C ter-
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