Suppression of KLF7 gene expression inhibits proliferation and induces apoptosis of hemangioma cells via NF-κB signaling pathway

Abstract

Purpose: To assess the role of Kruppel-like factor 7 (KLF7) in hemangioma (HA) progression, KLF7 expression and regulation of downstream targets in HA tissues and hemangioma-derived endothelial cells (HemECs) have been evaluated. Methods: Quantitative polymerase chain reaction (qPCR) and immunoblotting were performed to assess KLF7 expression in HA tissues and normal tissues. Endothelial cells were isolated from HA tissues, and Cell Counting Kit-8 assay and flow cytometry were carried out to analyze proliferation and apoptosis of the isolated HemECs. Immunoblotting was used to determine the effect of KLF7 on expression of members of nuclear factor kappa B (NF-κB) pathway in HemECs. Results: High KLF7 expression occurred in infantile HAs during the proliferative stage. Knockdown of KLF7 expression in HemECs inhibited proliferation and induced apoptosis via suppression of NF-κB pathway (p < 0.001). Conclusion: KLF7 is a promising therapeutic target for the treatment of HA.