Inhibition Of C-myc Oncogene By Small Interference RNA In Laryngeal Squamous Carcinoma Cells

Objective: To study the effect of the small interference RNA(the small interferingRNA, siRNA) in reducing the target c-myc oncogene expression for Hep-2 cell line inthe human Laryngeal Squamous Carcinoma by the interference RNA technology. Aswell as, chose the differential c-myc siRNA list for the preparation gene treatment.Method:1. On the basis of the principle of the c-myc oncogene standard sequence of siRNA,three interference sequences of c-myc oncogene were designed. The Hep-2 cells linewere transfected in growth period of siRNAs of the three sites separately, and theresults of RNAi were observed and measured in 48 hours later.2. The inhibition of c-myc oncogene was observed, targeted by the small interferenceRNA in Hep-2 cell in the Laryngeal Squamous Carcinoma, for the mRNA and cellexpression level by the way of the fluorescent quantitative RT-PCR and the MTT.3. The inhibition of c-myc oncogene targeted by the small interference RNA inHep-2 cell in the Laryngeal Squamous Carcinoma was observed in cell morphologyobservation by phase contrast microscope, HE staining and transmission electronmicroscope.Results:1. The result of the real-time quantitative PCR (polymerase chain reaction) showedthe expression decreased of the c-myc at mRNA level compared with the negativegroup and the bank group. Inhibition rate was at 94% in group S3. The result of theMTT showed the target c-myc siRNA to be able effectively to suppress themultiplication of Hep-2 cell line. The livability of group S3 was 77% comparingwith the negative group. 2.The morphology result showed the c-myc siRNA to be able effectively tosuppress multiplication of the Hep-2 cell, the oncogenic cell heteromorphism wasdiminished.Conclusion:1. Specific siRNA can effectively repress the expression of c-myc oncogene inHep-2 cells in the level of mRNA and cell.2. Expressions of repressing c-myc oncogene csn inhibit the proliferation of Hep-2cell and induce apoptosis. It indicates that c-myc oncogene can be as target point fortumor gene therapy.