CCDC50 suppresses NLRP3 inflammasome activity by mediating the autophagic degradation of NLRP3

Autophagy and autophagy-associated genes are closely linked to NLRP3-mediated inflammation in inflammatory disorders. This study determined that the functions of CCDC50, the novel autophagy receptor, in regulating the activation of NLRP3 inflammasome and associated inflammatory diseases. We performed transcriptome profiling (RNA-seq) and quantitative reverse transcription polymerase chain reaction (qRT–PCR) in shCtrl and shCCDC50 cells to evaluate the inflammatory responses regulated by CCDC50. The deep sequencing results showed that CCDC50 defciency caused increased NLRP3 inflammasome assembly and upregulation of associated disease pathways. Overall design: Immune signaling pathways-competent A375 cells were transduced with lentivirus carring shCtrl or shCCDC50 plasmids. The infected cells were selected with puromycin for 7 days. The deletion of CCDC50 was confirmed by qRT-PCR and immunobloting. The shCtrl and shCCDC50 cells were collected for mRNA profilling analysis.