Figure 6. PPARγ inverse agonists suppress tumor growth in xenograft models of salivary MEC.

(A) Growth of HMC3A xenograft tumors over time during treatment with either SR10221 or vehicle control. Tumor xenograft volume was quantified by caliper measurements obtained on the indicated days following initiation of drug administration. Decreased tumor volume in the SR10221 cohort correlates directly with suppression of tumor growth in vivo (n = 4, mean ± SEM; Student’s t test; ****p ≤0.0001).

(B) Weight of resected vehicle- and SR10221-treated HMC3A tumor xenografts at the study endpoint (n = 4, mean ± SEM; Student’s t test; **p ≤ 0.01).

(C) Representative in vivo bioluminescent images obtained at the endpoint of Nu/Nu mice bearing subcutaneous HMC3A tumor xenografts and treated with either SR2595 or vehicle control. Images were captured with an open filter and an acquisition time of 5 min (binning = 2; FOV = 25; Fstop = 2; object height = 1.5).

(D) Weights of Nu/Nu mice bearing subcutaneous HMC3A xenograft tumors and treated with SR2595 or vehicle control for up to 24 days (n = 4, mean ± SEM). (E) Comparison of HMC3A xenograft tumor growth following treatment with either SR2595 or vehicle control. Bioluminescence imaging (BLI) signals from tumor xenografts were quantified by region of interest (ROI) analysis of images obtained at the endpoint (day 24 following initiation of drug administration). A decreased BLI signal in the SR2595 cohort correlates directly with suppression of tumor growth in vivo (n = 4, mean ± SEM; Student’s t test; **p ≤ 0.01).

(F) Volume of resected vehicle- and SR2595-treated HMC3A xenograft tumors at the study endpoint (n = 4, mean ± SEM; Student’s t test; *p ≤ 0.05).

(G) Weight of resected vehicle- and SR2595-treated HMC3A xenograft tumors at the study endpoint (n = 4, mean ± SEM; Student’s t test; *p ≤ 0.05).