Abstract: Objective To explore the effect of GATA binding protein 3 on the migration abilityof breast cancer cells. Methods Lentivirus-mediated GATA3-knockdown cell line was establishedto study the expression levels and function of GATA3 by performing real-time quantitative fluorescentPCR, Western blotting and Transwell assay in vitro. The binding sites of GATA3 in LIFR promoterregion was detected by Chromatin immunoprecipitation assay ( ChIP-qPCR) assay in MCF7 andT47D cells. LIFR was overexpressed in MCF7 cells with reduced GATA3 expression, and the migration capacity of MCF7 cells was measured by Wound healing assay and Transwell assay. Results Compared with the control group, the group of MCF7 cells that knocked down GATA3 had enhancedmigration ability (all P< 0. 05), and decreased expression of LIFR ( all P < 0. 05). ChIP-qPCRdata showed a physical binding of GATA3 on the promoter region of LIFR in MCF7 and T47D cells(all P< 0. 05). Overexpression of LIFR rescued the enhanced cell migration induced by depletion of GATA3 in MCF7 cells (all P< 0. 05). Conclusion GATA3 inhibits the migration of breast cancercells MCF7 through transcriptional activation of LIFR.

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