KLF17 Protein Expression In Esophageal Squamous Carcinoma And Its Function On Migration And Invasion Of Eca109 Cells

ObjectiveTo discuss KLF17 protein expression in esophageal squamous carcinoma and their relationship between clinical and pathological factors; To investigate functions and mechanism on migration and invasion of Eca109 cells caused by KLF17.MethodsKLF17 protein expression in 44 esophageal squamous carcinoma and 37pericarcinomanormal tissues were detected by immunohistochemical stain.Built carrier of KLF17-lentivirus which infect Eca109 cells with different MOI,choosing suitable MOI according to GFP expression; KLF17 mRNA expression was detected by real-time PCR; KLF17、E-cadherin、 N-cadherin protein expression were detected by western blotting; Migrative ability were observed by wound-healing assay; invasive capacity were observed by transwell assay.ResultKLF17 protein expression in esophageal squamous carcinoma were remarkable lower than in pericarcinomanormal tissues (P<0.05); The rate of KLF17 negative was positively related to infiltration depth, lymph node metastasis and TNM stages (P<0.05); Transfection efficiency surpassed 95% when choosing MOI=50; RT-PCR and western blotting showed KLF 17 mRNA expression, KLF 17 and E-cadherin protein expression in Ad-KLF 17 group were increased significantly than others while N-cadherin protein expression was on the contrary after infection. Wound-healing assay showed the migration distance of Ad-KLF17 group was (137.2±8.24) um, remarkblely shorter than d-GFP group (228.6±22.48) um and CON group (221.4±25.92) um (P<0.05). Transwell assay showed the cellsnumber of Ad-KLF17 groupwent through venticles were 27±3.2,remarkably less than Ad-GFP group54.2±4.3 and CON group 58±4.5(P<0.05).ConclusionKLF 17 play a important role in esophageal squamous carcinoma associated with accurrence and progression; KLF 17 protein expression in esophageal squamous carcinoma were remarkable lower than in pericarcinomanormal tissues and related to infiltration depth, lymph node metastasis and TNM stages. EMT could be inhabited in Eca109 cells by overexpress KLF 17, associated with their migrative and invasive capacity.