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. 2016 Mar 14;7(17):23552–23568. doi: 10.18632/oncotarget.8083

Figure 5. The upregulation of CXCR4 by KLF8 leads to a feed-forward activation of FAK upstream of KLF8.

Figure 5

(A) Overexpression of KLF8 causes CXCL12/CXCR4-dependent activation of FAK. Uninduced (U) and induced (I) 10A-iK8 cells were serum-starved for 24 hours followed by 3-hour treatment with AMD3100 (35 ng/ml) or mock treatment prior to CXCL12 (100 ng/ml) stimulation. Whole cell lysates were prepared for western blotting for FAK phosphorylation at Y397 (pFAK) and total FAK. (B) Overexpression of KLF8 induces CXCL12/CXCR4-dependent expression of endogenous KLF8. The 10A-iK8 cells were grown and treated similarly as in A except for inclusion of PF223, a FAK-specific inhibitor. Total RNA was prepared for qRT-PCR (top panel) and semi-quantitative RT-PCT (bottom panel). (C) Hypothetic model for the feed-forward signaling loop of KLF8 to CXCR4/CXCL12 to pFAK and back to KLF8.