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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: Gastroenterology. 2015 Nov 12;150(3):707–719. doi: 10.1053/j.gastro.2015.11.002

Figure 7. Twist1 overexpression drives tumor growth independently of Tlr4.

Figure 7

TICs were transduced with lentivirus expressing shRNA for Tlr4 or scrambled shRNA followed by a second transduction with retrovirus expressing Twist1 overexpression (OE) plasmid vector or empty vector (Emp). These cells were injected subcutaneously into the rear flanks of NOG mice (1 million cells/injection). (A) Tumor volume measured at day 15, 25 and 30 (also whenever an unexpected death occurred) demonstrated an increasing trend in the tumor volume with intact Tlr4 and Twist1 overexpression when compared to their respective controls (sh-Tlr4+OE vs sh-Tlr4+Emp; ***, P<0.001; n=4 NOG mice/cohort; n=2; statistics performed using 2-way ANOVA). (B) Significant increase in the overall tumor weight (***, P<0.001, ****, P<0.0001, n=4 NOG mice/cohort; n=2). (C) Overexpression of Twist1 promotes Liver and Lung metastasis irrespective of the endogenous Tlr4 expression in TICs. (D) A schematic representation of the proposed link between oncogenic TLR4/NANOG signaling, OB-R/pSTAT3 and an effective TWIST1 pathway in generating TICs.