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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: J Thromb Haemost. 2021 Jul 19;19(10):2480–2494. doi: 10.1111/jth.15440

Figure 7: Proposed model explaining fibrinogen-driven colon cancer growth.

Figure 7:

Fibrinogen/integrin interactions in the TME leads to FAK activation, ultimately leading to the degradation of p53 and downregulation of downstream p53 targets (14-3-3σ and p21), thereby promoting cell proliferation and survival. In the absence of fibrinogen, p53 is stabilized leading to increased expression of its downstream targets, resulting in cell senescence and growth inhibition.