Latest revision as of 06:45, 4 August 2019

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DESCRIPTION

Overall Introduction

Based on the high heterogeneity and invasiveness of TNBC, our team has characterized a gene circuit with three modules. Controlled by TNBC-specific promoter 1, module 1 includes a miRNA binding site(BS) and a transcription factor which drives Module3 --- expression of a fusion protein composed of HIF1-αoDDD and yeast cytosine deaminase (yCD) working under hypoxia conditions. Module 2 includes several sponge-like domains effectively down-regulating specific miRNA when promoter 2 is driven. Supposing the miRNA is highly expressed in the normal cells and low in most cancer cells, this circuit could trigger highly selective cytotoxicity of cancer cells. Once optimized, our design could be applied to current treatments, allowing for a more powerful therapeutic effect with a comparatively low risk.

Status 1(in TNBC cells)

High efficiency of P1 + low miRNA expression + hypoxia=kill

Status 2(in TNBC cells)

High efficiency of P1&P2 + relatively high expression of miRNA + hypoxia=kill

Status 3(in normal cells)

Little expression of GAD nor sponge=not kill

Status 4(in normal cells)

Relative high efficiency of P1 + low efficiency of P2 +high level of miRNA + normoxia=not kill

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