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. 2022 Mar 4;14(5):1315. doi: 10.3390/cancers14051315

Figure 9.

Figure 9

Figure 9

Synthetic lethal effect between CaMKII and NK1R inhibitors on GSCs is associated with the inhibition of PI3K/AKT/NF-κB and calcium signaling. (A) Effect of CaMKIIγ knockdown on NK1R expression in U87MG- and U373MG-derived GSCs. (B) Effect of NK1R knockdown on CaMKIIγ expression in both GSCs. p < 0.05 vs. the control siRNA. (C) Effect of combined treatment (12 h) of CaMKII and NK1R inhibitors on PI3K/AKT/NF-κB pathway in both GSCs. (D) Effect of concurrent knockdown of CaMKIIγ and NK1R on PI3K/AKT/NF-κB pathway in both GSCs. (A–D) Protein levels were detected by Western blot analysis using specific antibodies and were further quantified by densitometry. β-actin levels were used as an internal control. Original Western blots are shown in Figure S1. (E) Effect of combined treatment (12 h) of CaMKII and NK1R inhibitors on intracellular calcium level in both GSCs. The levels of calcium were detected with Fluo-4 AM using a fluorescence microscope and were further quantified using a multimode microplate reader. * p < 0.05, ** p < 0.01 vs. the compound alone or the single gene knockdown.