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. 2021 Sep 4;24(9):103086. doi: 10.1016/j.isci.2021.103086

Figure 7.

Figure 7

OSCC-derived DDX3 mutants have greater potential to induce AREG expression

(A) Schematic representation of human DDX3 protein as in Figure 4C, in which OSCC-derived mutations are indicated.

(B) In vivo translation assays were performed as Figure 4C, except that FLAG-tagged wild-type or DDX3 mutant was overexpressed. Bar graph shows relative hRL/hFL activity (mean ± SD); ∗p < 0.01.

(C) Immunoblotting of the lysates of SAS cells that were transfected with siD#1 and the indicated expression vectors.

(D) SAS cells were transfected with the expression vector encoding GFP-tagged wild-type or mutant DDX3 (in order to distinguish transiently expressed DDX3 from the endogenous). Immunoblotting of anti-SRP54-coimmunoprecipitates was performed using antibodies against GFP or SRP proteins as indicated. Bars represent IP/Input ratios of DDX3 blots (mean ± SD; ∗p<0.01).

(E) OSCC-associated mutant DDX3 increases the expression of AREG, which exerts both autocrine and paracrine activities and hence promotes TME remodeling.