Abstract Total triterpenoids from Antrodia cinnamomea fermentation mycelium (TT-ACFM) were prepared, and their in vitro inhibitory effects on hepatocellular carcinoma were investigated. Human hepatocellular carcinoma HepG2 cells were incubated with TT-ACFM with concentration of 0 (control), 12.5, 25, 50, 100 and 200 μg/mL, respectively. The proliferation of cell was detected using CCK-8 method. The apoptosis of cells was detected by flow cytometry. The migration and invasion of cells was determined using Transwell chamber. The level of reactive oxygen species (ROS) in cells was determined using DCFH-DA method. The expressions of matrix metalloproteinse-2 (MMP-2), matrix metalloproteinse-9 (MMP-9) and vascular endothelial growth factor (VEGF) protein in cells were detected by western blot assays. Results indicate that, TT-ACFM can not only inhibit the proliferation of HepG2 cells and promote their apoptosis, but also inhibit their invasion and invasion. The mechanism may be related to its increase of ROS and down-regulation of MMP-2, MMP-9 and VEGF expression in cells.

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.