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. 2019 Feb 21;27(3):359–369. doi: 10.3727/096504018X15220594629967

Figure 7.

Figure 7

BCAR4 promoted NSCLC cell proliferation, migration, and invasion by regulating GLI2. (A) The expression levels of GLI2 downstream proteins were remarkably higher in the BCAR4 overexpression group, while the levels of GLI2 downstream proteins were much lower in the si-GLI2 group. The expression levels of the proteins in the BCAR4 + si-GLI2 group showed no significant difference from those in the NC group. *p < 0.05, compared with the NC group; #p < 0.05, compared with the si-GLI2 group; +p < 0.05, compared with the BCAR4 group. (B) Cell viability in the BCAR4 overexpression group was dramatically improved, while cell viability in the si-GLI2 group was suppressed. *p < 0.05, compared with the NC group; #p < 0.05, compared with the si-GLI2 group; +p < 0.05, compared with the BCAR4 group. (C) The wound healing area in the BCAR4 overexpression group was manifestly larger, whereas the wound healing area in the si-GLI2 group was much smaller. *p < 0.05, **p < 0.01 compared with the NC group; #p < 0.05, compared with the si-GLI2 group; +p < 0.05, compared with the BCAR4 group. (D) There were notably more invaded cells in BCAR4 overexpression group, while much fewer invaded cells were observed in the si-GLI2 group. *p < 0.05, compared with the NC group; #p < 0.05, compared with the si-GLI2 group; +p < 0.05, compared with the BCAR4 group.