prostate cancer;
DNA methylation;
DNMT3;
RNA interference;
MAMMALIAN DNA METHYLTRANSFERASES;
RNA INTERFERENCE;
GASTRIC-CANCER;
METHYLATION;
HYPERMETHYLATION;
EXPRESSION;
EPIGENETICS;
INHIBITOR;
GROWTH;
3B;
D O I:
10.1590/S1415-47572012005000021
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
070307 [化学生物学];
071010 [生物化学与分子生物学];
摘要:
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.