The Research Of Knockdown Of STAT3by RNAi Efficiently Induce Colon Cancer Sw620Apoptosis And The Mechanism

Aim: Signal transducer and activator of transcription3(STAT3) is anuclear transcription factor which is also a point of convergence fornumerous oncogenic signaling pathways, including tumor cell apoptosis,cell cycle, cell invasion and tumor angiogenesis. Colorectal cancer is one ofthe most common malignant tumor worldwide, which is the second leadingcause of death malignancies in the40-79year-old population of the UnitedStates. RNA interference (RNAi) is a specific posttranscriptional genesilencing mechanism which could efficiently inhibit the expression ofprotein-coding genes and now widely used as a tool in gene silencing, drugdiscovery and gene therapy. In our study, we silence the protein of STAT3expression in sw620tumor cells by RNAi. Then we studied the antitumoreffect and mechanism in vitro.Methods: In this study, short hairpin RNA targeting STAT3was clonedinto pGenesil-1plasmid vector, named as p-shSTAT3. Forty-eight hoursafter transfection with p-shSTAT3, the expression level of STAT3mRNAand protein were measured using RT-PCR and Western blot. Moreover, Hochest33258staining was used to measure the apoptosis of sw620cellafter transfection. Furthermore, downstream apoptosis-related targets ofSTAT3in sw620cell was investigated by Western blot.Results: Our results indicated that p-shSTAT3could significantlysilence STAT3mRNA and protein expression in sw620cancer cells.Hochest33258staining indicated that p-shSTAT3induced the sw620cancercell apoptosis. We found knockdown of STAT3expression induce p53、Caspase3and Bax protein expression, and ainhibit Bcl-xL and Bcl-2proteinexpression in sw620cells.Conclusion: Our data showed that knockdown of STAT3expressioninduced p53、Caspase3and Bax protein expression, inhibited Bcl-xL andBcl-2protein expression in sw620cells and produced anti-tumor effects ofinducing the sw620apoptosis. It provide new ideas and targets of treatmentfor colon cancer.