NF-κB p65 Subunit Is Modulated by Latent Transforming Growth Factor-β Binding Protein 2 (LTBP2) in Nasopharyngeal Carcinoma HONE1 and HK1 Cells

摘要: NF-κB is a well-characterized transcription factor, widely known as key player in tumor-derived inflammation and cancer development. Herein, we present the functional molecular relevance of canonical p65 subunit nasopharyngeal carcinoma (NPC). Loss- gain-of-function approaches were utilized to reveal characteristics propagating tumor growth, tumor-associated angiogenesis, epithelial-to-mesenchymal transition NPC cells. Extracellular inflammatory stimuli are critical factors that trigger signaling; hence, investigated components microenvironment might potentially influence signaling pathway. This led identification an extracellular matrix (ECM) protein was previously reported candidate suppressor NPC. Our studies on Latent Transforming Growth Factor-β Binding Protein 2 (LTBP2) provides substantial evidence it can modulate transcriptional activity. Re-expression LTBP2 elicits suppressive effects parallel inactivation able reduce phosphorylation at Serine 536, inhibit nuclear localization active phosphorylated p65, impair DNA-binding ability. results consequential down-regulation p65-related gene expression. Therefore, data suggest overall up-regulation expression loss this ECM milestone events contributing