The aim of the present study was to investigate the effect of phosphoinositide-specific phospholipase Cε (PLCε) gene silencing on the inhibition of cancer development in ulcerative colitis (UC) and to explore the pathogenesis and carcinogenic mechanism of UC, in order to facilitate the establishment of novel strategies for the treatment of UC, prevent the cancerous transformation of UC and discern the association between inflammation and cancer. A pGenesil-PLCε RNA interference vector was constructed and transfected into HEK293 cells (pGenesil-PLCε group). HEK293 cells transfected with pGenesil empty plasmid were set as the negative control (pGenesil-NC group). The expression of PLCε was observed, and molecules associated with the PLC signaling pathway were detected using a reverse transcription-quantitative polymerase chain reaction and western blotting. ELISA was used to determine the expression of serum interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) of mice in which the PLCε gene had been silenced. Compared with the pGenesil-NC group, the mRNA and protein levels of PLCε were significantly decreased in the pGenesil-PLCε group. In addition, the mRNA levels of K-ras, NF-κB, Fas and Bcl-2 were markedly reduced, while P53 mRNA level was notably enhanced, in the pGenesil-PLCε group, and these changes were accompanied by similar changes in the corresponding protein levels. The serum IL-1 and TNF-α expression in the PLCε gene-silenced mice was significantly reduced compared with that in the control mice. In conclusion, PLCε RNA silencing can effectively inhibit the cancerous transformation of UC by regulating the colorectal cancer-related cell proliferation and cell cycle in vivo. In addition, PLCε RNA silencing can suppress the expression of inflammatory factors in vitro.
Keywords: RNA silencing; canceration; inflammation; phosphoinositide-specific phospholipase Cε; ulcerative colitis.