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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Cancer Res. 2021 May 3;81(13):3607–3620. doi: 10.1158/0008-5472.CAN-20-3790

Figure 5. DDX3X helicase activity is critical for preventing accumulation of dsRNAs and dsRNAs-mediated type I IFN activation.

Figure 5.

A. J2 dot blot analysis with total RNAs extracted from MCF7 cells treated with RK-33 for 24 hours. A bar graph shows relative dsRNA dot intensity.

B. Western blot analysis in RK-33 treated MCF7 cells (24 hours and 72 hours).

C. qRT-PCR of IFNB1 in RK-33 treated MCF7cells (72 hours).

D. qRT-PCR of ISGs in RK-33 treated MCF7 cells (72 hours).

E. Western blot analysis of MDA5 and phospho-STAT1 in MDA5 KO MCF7 cells followed by RK-33 treatment (24 hours).

F. qRT-PCR of ISGs in DDX3X-KD MCF7 cells followed by overexpression of DDX3X mutants (G302V and K230E/E348Q).

G. Schema of the activation of dsRNA-mediated type I IFN signaling in DDX3X-KD or DDX3X-inhibited (RK-33) cancer cells.

Data are shown as mean ± SEM of three independent experiments. Statistical significance was calculated using unpaired t-tests (Fig. 5A, 5C, and 5D) or one-way ANOVA with uncorrected Fisher’s LSD test (Fig. 5F). *p < 0.05; **p< 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant.