LncRNA FAM225A activates the cGAS-STING signaling pathway by combining FUS to promote CENP-N expression and regulates the progression of nasopharyngeal carcinoma

Abstract

BackgroundNasopharyngeal carcinoma (NPC) is a common malignant tumor and long non-coding RNAs (lncRNAs) are widely involved in NPC development. Nevertheless, the role of lncRNA FAM225A in NPC remain unclear. Here, we evaluated the effect of FAM225A on NPC cell proliferation, migration and epithelial-mesenchymal transition (EMT). MethodsLevels of FAM225A and CENP-N in NPC tissues and cells were measured using RT-qPCR. Western blot assessed CENP-N, Snail, E-cadherin, N-cadherin, Vimentin, cGAS and p-STING levels. FAM225A expression was knocked down by sh-FAM225A or overexpressed by pcDNA-FAM225A. RIP and RNA pull-down verified the binding between FAM225A, CENP-N and FUS. Cell proliferation, migration and invasion were evaluated by CCK8, colony formation and transwell assays. ResultsFAM225A and CENP-N expression levels were evaluated in NPC tissues and cell lines. FAM225A knockdown inhibited NPC cell proliferation, migration and EMT. FAM225A stabilized CENP-N mRNA by recruiting FUS. FAM225A activated cGAS-STING by regulating the expression of CENP-N to promote NPC cell proliferation, migration and EMT. ConclusionFAM225A regulates NPC progression via FUS/CENP-N mediated cGAS-STING signaling pathway, which provides new therapeutic targets for developing new NPC treatments.