Fig. 2

A schematic illustration of the role of STAT3 signaling cascade in regulating CDK1 and CDK2 in lung cancer. Accumulating evidence has illustrated that CDK1/GP130/STAT3 signaling could promote lung cancer tumorigenesis. It has been reported that Iron-dependent CDK1 activity could phosphorylate 4E-BP1, which in turn elevates STAT3 signaling pathway via upregulation of GP130 [48]. Moreover, another research has revealed that PROS could downregulate VEGF induced proliferation, migration, and tube formation in non-small lung cancer cells and inhibits angiogenesis in chorioallantoic membrane assay through attenuating phosphorylation of VEGFR2, Src, and STAT3, thereby inducing sub G1 accumulation, S phase arrest [158]