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. 2023 Jun 17;10(24):2301505. doi: 10.1002/advs.202301505

Figure 3.

Figure 3

Activation of TGF‐β signaling in Bmal1−/− tumor and CAFs. A) ELISA quantification of active TGF‐β in CRC tumors and plasma from tumor‐bearing mice (n = 4 samples per group). B,C) Immunoblot and quantification of p‐SMAD2 and α‐SMA in CRC tumor and CAFs from Bmal1+/+ and Bmal1−/− mice (n = 4 samples per group). D) Cell motility and quantification (n = 5 colonies per group). Quantification of CAFs number after 48 h from Bmal1+/+ and Bmal1−/− mice (n = 4 random fields per group). E) Schematic diagram of activation of TGF‐β signaling. Tumor and tumor‐bearing host plasma provide resource of latent TGF‐β. Bmal1 deficiency augment PAI‐1‐uPA/tPA‐plasmin axis. High plasmin serves as activator convert latent TGF‐β into active form. Data presented as mean ± S.E.M. *P < 0.05; **P < 0.01; ***P < 0.001; two‐tailed student t‐test.