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Abstract：
In this study, we aimed to investigate the molecular mechanism of Krüppel-like factor 7 (KLF7) in colorectal cancer (CRC) cell invasion and migration. The expression pattern of KLF7 in CRC tissues and the correlation between KLF7 expression and clinical symptoms of CRC were analyzed. CRC cell lines were transfected with si-KLF7, followed by qRT-PCR or western blot detection of KLF7, miR-139-5p, and tumor protein D52 (TPD52) expression, cell counting kit-8 (CCK-8) assay to detect cell viability, and transwell detection of invasion and migration. Chromatin immunoprecipitation (ChIP) analyzed the enrichment KLF7 in the miR-139-5p promoter. The dual-luciferase reporter assay verified the binding relationship between KLF7 and miR-139-5p, and between miR-139-5p and TPD52. In the subcutaneous tumorigenesis experiment, tumor growth was observed and ki67-positive expression was detected. KLF7 is abundantly expressed in CRC cells KLF7 silencing inhibits CRC cell viability, invasion, and migration. KLF7 represses miR-139-5p expression by binding to the miR-139-5p promoter. miR-139-5p targets TPD52 expression. miR-13-5p inhibition or TPD52 overexpression partially counteracted the effect of KLF7 silencing in CRC cells. KLF7 silencing suppresses tumor growth in vivo. In conclusion, KLF7 suppresses miR-139-5p expression by binding to the miR-139-5p promoter, thereby upregulating TPD52 expression and enhancing CRC cell invasion and migration.
摘要：
在这项研究中,我们旨在探讨Krüppel样因子7（KLF7）在结直肠癌（CRC）细胞侵袭和迁移中的分子机制。分析KLF7在CRC组织中的表达模式以及KLF7表达与CRC临床症状的相关性。用si-KLF7转染CRC细胞系，然后qRT-PCR或蛋白质印迹检测KLF7，miR-139-5p，和肿瘤蛋白D52（TPD52）表达，细胞计数试剂盒-8（CCK-8）检测细胞活力，以及Transwell入侵和迁移的检测。染色质免疫沉淀(ChIP)分析了miR-139-5p启动子中的富集KLF7。双荧光素酶报告基因实验验证了KLF7与miR-139-5p的结合关系,以及miR-139-5p和TPD52之间。在皮下肿瘤发生实验中,观察肿瘤生长,检测到ki67阳性表达.KLF7在CRC细胞中大量表达KLF7沉默抑制CRC细胞活力,入侵,和移民。KLF7通过结合miR-139-5p启动子抑制miR-139-5p表达。miR-139-5p靶向TPD52表达。miR-13-5p抑制或TPD52过表达部分抵消了CRC细胞中KLF7沉默的影响。KLF7沉默在体内抑制肿瘤生长。总之,KLF7通过与miR-139-5p启动子结合抑制miR-139-5p表达，从而上调TPD52表达并增强CRC细胞侵袭和迁移。
