Fig. 5

LINC00669 negatively regulates STAT1 ubiquitination. a, Microarray data showing upregulation of the key JAK/STAT signaling pathway component genes in NPC tumors. b, Representative IHC results showing the aberrantly enriched STAT1 protein in NPC tumors in comparison to nasopharyngeal non cancer (NPNC) tissues. c, qPCR analysis showing neither SOCS1 nor STAT1 were subject to a changed with LINC00669 at transcription level. LINC, overexpression of LINC00669; siLINC, siRNA-mediated silencing of LINC00669. d, Western blotting showing STAT1 but not SOCS1 protein expression was regulated by LINC00668. Ectopic expression of LINC00669 increased STAT1 protein amount while depletion of LINC00668 decreased STAT1 protein abundance. e, Co-IP assay showing endogenous STAT1 ubiquitination was dramatically increased upon knockdown (KD) of LINC00669 in NPC cells. Ubi, ubiquitin. Normal IgG was used as a negative control for IP. f, Co-IP assay showing exogenous ubiquitination modification on GFP-fused STAT1 protein was dramatically diminished upon overexpressing LINC00669