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. 2019 Sep 26;11(10):1442. doi: 10.3390/cancers11101442

Figure 3.

Figure 3

LCC-09 suppressed the viability and metastatic phenotype of GBM cells through the dysregulation of DRD4-mediated AKT/mTOR and NF-κB signaling axes. (A) LCC-09 significantly suppressed the viability of TMZ-resistant CD133+ U87MG and D54MG cells in a dose-dependent manner. Photo-images and graphical representation of the inhibitory effect of LCC-09 on the ability of TMZ-resistant CD133+ U87MG and D54MG cells to (B) form colonies, and (C) migrate. (D) LCC-09 downregulates the expression level of DRD4, β-catenin, Akt, mTOR, NF-κB, Erk1/2, c-Myc, and CDK6 proteins in TMZ-resistant CD133+ U87MG and D54MG cells compared to their vehicle-treated counterparts. β-actin served as loading control. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant; Data represent the mean ± SD of experiments performed 4 times in triplicates.