Fig. 5: LCK functions as a downstream target gene of ATMIN in NPC cells.
From: Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma
A Western blot analysis of LCK expression after ATMIN silencing. B ATMIN-binding motif and predicted LCK promoter site binding for ATMIN. C ChIP-qPCR validation of ATMIN enrichment on the promoter of LCK. D Dual-luciferase reporter assays in HONE1 and SUNE1 cells co-transfected with ATMIN plasmid or empty vector and pGL3-Basic-LCK plasmid (n = 3). E CCK-8 assays determining the growth curves of HONE1 and SUNE1 cells co-transfected with si-NC plus vector or si-ATMIN#1 plus vector or si-ATMIN#1 plus LCK plasmid. F Representative images and quantification of the colony formation assays in HONE1 and SUNE1 cells co-transfected with si-NC plus vector or si-ATMIN#1 plus vector or si-ATMIN#1 plus LCK plasmid. G CCK-8 assays in HONE1 and SUNE1 cells co-transfected with si-NC plus vector or si-ATMIN#1 plus vector or si-ATMIN#1 plus LCK plasmid followed with docetaxel treatment in an increased dose manner. Data are presented as mean ± SD, P values were calculated using Student’s t test (C, D) or one-way ANOVA (E–G). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. The unprocessed images of the blots are shown in Supplementary Fig. S3.
