Roles Of HMGA1in E-cadherin Expression Regulation In Thyroid Cancer Cells

Objective: To investigate the effect of HMGA1on E-cadherin expression in thyroidcancer cells, and to unveil the underling mechanism.Motheds: To assess the effect of HMGA1on the expression of E-cadherin,Western-blot were used. siRNA interference technology was performed to knockdownthe expression of HMGA1in thyroid cancer cells. Luciferase reporter assay wasutilized to analyze the effect of HMGA1on E-cadherin promoter activity. The effectof HMGA1on thyroid cancer cell invasion ability was determined by transwellexperiment.Results:1. Compared with control group and scramble siRNA group, the HMGA1level in SW579cells was decreased when treated with HMGA1/siRNA for40nmol/L,80nmol/L and160nmol/L, and HMGA1reached the lowest level when treated for160nmol/L(p<0.05). Compared to control group and scramble siRNA group, theE-cadherin level in SW579cells was increased when treated with HMGA1/siRNA for40nmol/L,80nmol/L and160nmol/L, and E-cadherin showed highest expression whentreated with160nmol/L of HMGA1/siRNA(p<0.05).2. A Luciferase reporter plasmid with a proximal promoter region (-306-+57)of E-cadherin was successfully established and showed the promoter activity inthyroid cancer cells. Luciferase reporter assay showed that HMGA1could decreasethe promoter activity of E-cadherin in both SW579and TPC-1cells, and2μg ofpcDNA3.1/HMGA1showed the highest inhibitory effect on the promoter activity ofE-cadherin compare to pGL4.10-E-cadherin group(p<0.05).3. Transwell experiment showed that HMGA1/siRNA induced downregulation of HMGA1could lead to a decrease of invasion ability of SW579cellscompared to the scramble siRNA transfected cell group and control group(p<0.05). Conclusions:1. HMGA1could enhance invasion ability of SW579cells.2. HMGA1could negatively regulate the expression of E-cadherin inthyroid cancer cells by suppressing E-cadherin promoter activity.