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. 2017 Mar 23;8(20):33353–33364. doi: 10.18632/oncotarget.16495

Figure 3. ArpC inhibition impaired the stemness marker expression, Notch activity, and self-renewal ability of CD133+ U87-MG and U251-MG glioma neurospheres.

Figure 3

(A) Cells were treated by ArpC specific inhibitor CK636 for 24 hours. Cell viability was determined by Trypan Blue assay. (B) CD133+ cells were cultured in 10% serum-containing medium to induce lamellipodia. The suppression of lamellipodia formation was observed through confocal microscope after CK636 (2μM) treatment for 30 minutes (Orange: actin filaments, Blue: Nucleus). (C) HES1 expression was determined after CK636 treatment for 24 hours with different doses. (D) HES1 expression was measured after CK-636 (2μM) treatment for different periods. (E) Protein expression was detected by Western blot after shArp2 and CK636 (2μM) treatment for 24 hours.