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. Author manuscript; available in PMC: 2020 Nov 25.
Published in final edited form as: FASEB J. 2020 Apr 18;34(6):7345–7359. doi: 10.1096/fj.201903033R

FIGURE 8.

FIGURE 8

Targeting Diaph1 or Rab5a suppresses myofibroblastic activation of HSCs and HSC-derived tumor-promoting factors in vivo. A,B, Tumor nodules, as described in Figure 7C, were subjected to WB. In the tumors arising from HT29/HSC-Diaph1shRNA or HT29/HSC-Rab5ashRNA coinjections, the protein levels of α-SMA, CTGF, PD-L1, IGF-1, and tenascin C were significantly reduced, compared to those in the tumors arising from control coinjections. *P < .05 by ANOVA, n = 5, 6. IF for α-SMA and tenascin C were also shown in A, lower panels. *P < .05 by t test, n = 4. Bar, 50 μm. C, Schematic presentation of the finding of this study that the Diaph1-Rab5a axis promotes the internalization of TGFβ receptors and myofibroblastic activation of HSCs