Generation of viable loss-of-function REH B-ALL cell models in which FBXW7 isoforms were transiently knocked down. (A) MO designed to target junctions of FBXW7 alternative first coding exons and corresponding downstream introns for transient isoform KD. (B) Reduction of FBXW7 transcripts by MO in an isoform-specific manner. Mixed primer RT-PCR was performed following FBXW7 KD in REH cells. FBXW7α and β transcripts were detected while γ was below detection limit in the 30-cycle PCR. (C) Taqman qPCR performed on REH cells following FBXW7 isoform KD. Error bars represent means ± SE of 2 independent experiments. One-way ANOVA of all groups was performed followed by Dunnett comparisons between the MO ctrl and other groups. ∗Adjusted P < .05, ∗∗adjusted P < .01. (D-E) Lack of effects on cell cycle progression of transient FBXW7 isoform KD in REH B-ALL cells. (F-G) Lack of effects on cell viability of transient FBXW7 isoform KD in REH B-ALL cells. An independent MO-ctrl–treated sample was serum-starved overnight, acting as a dead-cell positive control. Data representative of 2 independent experiments are shown in panels B, D, and F. Data represent means ± SEM of 2 independent experiments in panels E and G. One-way ANOVA was performed, and no significant difference was found between these groups.