Department of Ophthalmology, The People's Hospital of Danyang; Affiliated Danyang Hospital of Nantong University, Danyang, Jiangsu Province, China.
Department of Ophthalmology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Bioengineered. 2021 Dec;12(1):4374-4384. doi: 10.1080/21655979.2021.1953901.
The epithelial-mesenchymal transition (EMT) of lens epithelial cells enhanced their proliferation and migration and therefore induced the occurrence of posterior capsule opacity (PCO). Some studies revealed that Krüppel-like factor 1 (KLF1) promoted the proliferation and invasion of multiple types of cancer cells. Besides, the expression of KLF1 was elevated in the crystalline lens of cataract patients. However, the effect of KLF1 on the development of PCO remains unclear. In this study, TGF-β2 was used for the stimulation of human lens epithelial cell line to establish EMT (SRA01/04). The KLF1 was overexpressed and knocked down in SRA01/04 cells, the proliferation, migration and invasion of which were detected by clone formation assay, wound healing and transwell assay. In addition, ZBTB7A was overexpressed in KLF1-knocked down SRA01/04 cells, the proliferation and invasion of which were also measured by clone formation assay and transwell assay. KLF1 overexpression promoted the proliferation, migration and invasion of SRA01/04 cells. Moreover, KLF1 also promoted the expression of Vimentin, snail and α-SMA in SRA01/04 cells. KLF1 enhanced the expression of ZBTB7A and β-catenin, resulting in activation of ZBTB7A and Wnt/β-catenin signaling, while overexpression of ZBTB7A abolished the inhibitory effect of knocking down KLF1 on proliferation and invasion of SRA01/04 cells. These results indicated that KLF1 promoted the proliferation, migration and invasion of human lens epithelial cells by activating ZBTB7A and Wnt/β-catenin signaling pathway.
上皮-间充质转化（EMT）增强了晶状体上皮细胞的增殖和迁移能力，从而导致后囊膜混浊（PCO）的发生。一些研究表明，Krüppel 样因子 1（KLF1）促进了多种类型癌细胞的增殖和侵袭。此外，白内障患者晶状体中 KLF1 的表达水平升高。然而，KLF1 对 PCO 发展的影响尚不清楚。在本研究中，使用 TGF-β2 刺激人晶状体上皮细胞系建立 EMT（SRA01/04）。在 SRA01/04 细胞中过表达和敲低 KLF1，通过克隆形成试验、划痕愈合试验和 Transwell 试验检测细胞的增殖、迁移和侵袭能力。此外，在敲低 KLF1 的 SRA01/04 细胞中过表达 ZBTB7A，通过克隆形成试验和 Transwell 试验测量细胞的增殖和侵袭能力。KLF1 过表达促进了 SRA01/04 细胞的增殖、迁移和侵袭。此外，KLF1 还促进了 SRA01/04 细胞中波形蛋白、snail 和 α-SMA 的表达。KLF1 增强了 ZBTB7A 和 β-连环蛋白的表达，导致 ZBTB7A 和 Wnt/β-连环蛋白信号通路的激活，而过表达 ZBTB7A 则消除了敲低 KLF1 对 SRA01/04 细胞增殖和侵袭的抑制作用。这些结果表明，KLF1 通过激活 ZBTB7A 和 Wnt/β-连环蛋白信号通路促进人晶状体上皮细胞的增殖、迁移和侵袭。
