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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Ann N Y Acad Sci. 2015 Apr 15;1353(1):72–88. doi: 10.1111/nyas.12758

Figure 7.

Figure 7

Differential effects of miRNAs in kidney fibrosis and epithelial to mesenchymal transition (EMT) in cancer metastasis. In the early stage of DN, TGF-β1 induced by diabetic conditions upregulates miR-192 in mesangial and other renal cells through the activation of Smad 2/3, p53, or via Ets-1-mediated mechanisms. MiR-192 induces collagens by inhibiting E-box repressors (Zeb1/2) and also via increases in miR-200 family members. The miR-200 family also enhances collagen expression by targeting Zeb1/2 to amplify the signaling. On the other hand, in epithelial cancer cell lines or immortalized epithelial cell lines that have mutation in genes such as p53, Smads or Ets-1, TGF-β1 decreases miR-192. This also leads to decreases miR-200 family and E-Cadherin genes through E-box repressors (Zeb1/2) to induce EMT. Renal cell–specific transcription factors (such as HNF) can also be critical for cell-specific regulation of miRNAs in response to TGF-β1.