Abstract: Objective To explore the impact of silencing PLCε1 gene on proliferation and cell cycles of esophageal carcinoma Eca109 cells. Methods Three plasmid expression vectors (PLCε11, PLCε12 and PLCε13) were constructed to silence PLCε1 gene. A negative control plasmid expression vector (HK) was constructed at the same time to serve as control. The plasmid expression vectors were transfected into esophageal carcinoma Eca109 cells by cations liposome. The plasmid expression vector with the best interference effect (PLCε12) was chosen. The study included Eca109 group, HK group and PLCε12 group. Cell viability of Eca109 cells were evaluated by MTT assay. The cell cycles were detected by FCM. The mRNA expression of P16 and CyclinD1 gene were measured by RT-PCR. Results The cell viability of Eca109 cells in PLCε12 group were 80.73% and 75.88% at 48h and 72h after transfection, which were significantly lower than that of Eca109 cells in HK group (P<0.001). The percentage of S phase Eca109 cells in PLCε12 group was lower than that of Eca109 cells in HK group (P<0.01), the cell cycle of PLCε12 group Eca109 cells was arrested in G0/G1 phase. The P16 gene mRNA expression of PLCε12 group Eca109 cells was higher than that of HK group Eca109 cells (P<0.01). Conclusions Silencing PLCε1 gene might up-regulate P16 gene mRNA expression, arrest the cell cycle in G0/G1 phase and inhibit the proliferation of Eca109 cells.

Key words: PLCε1 gene, Esophageal carcinoma, RNA interference, Proliferation