Study On The Mechanism Of Arsenic Trioxide On Regulation Of HTERT Gene Promoter And Related-transcription Factors NF-κB In HL-60Cells

Objective: To study the mechanism of arsenic trioxide (As2O3) on HL-60cells hTERTgene promoter and related transcription factor NF-κ B。Method:1. Applying differentconcentrations of As2O3on HL-60cells, by using Real-time PCR and Western blottingmethods to detect respectively the change of hTERT and NF-κ B on mRNA and theprotein level.2.,we used Real-time PCR and Western blotting methods to detectrespectively the change of hTERT and NF-κ B on mRNA and the protein levelSimultaneously used CCK-8analysis method and Flow cytometry to detectrespectively proliferation activity and apoptosis change of HL-60cell after using RNAitechnology interfering NF-κB expression.Results:1. After different concentrations of As2O3are applied to HL-60cells, hTERTand NF-κB expression was significantly inhibited on mRNA and protein level (P<0.01).2. Silence the expression of the transcription factor NF-κB,and then hTERT, NF-κBwas significantly inhibited on mRNA and protein levels(P<0.01).3. Silence theexpression of the transcription factor NF-κB can effectively inhibit the proliferation ofHL-60cells obviously decreased (P<0.01),the most significant in48h after interfering.4.Silence the expression of the transcription factor NF-κB can effective to promoteapoptosis of HL-60cells (P<0.01).Conclusions:1. After being applied to HL-60cells, different concentrations of As2O3can promote apoptosis of HL-60cells, showing a certain dose-effect relationship.2.Silencing the expression of transcription factors NF-κ B can promote apoptosis andinhibit proliferation of HL-60cells.