The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
MiR-21/Smad 7 signaling determines TGF-β1-induced CAF formation
Open accessAbstract
How TGF-β1-mediated signaling pathways are finely tuned to orchestrate the generation of carcinoma-associated fibroblasts (CAFs) is poorly understood. Here, we demonstrate that miR-21 and the signaling of its target Smad 7 determine TGF-β1-induced CAF formation. In primary cultured fibroblasts, mature miR-21 increases after TGF-β1 treatment, whereas the Smad 7 protein level decreases. MiR-21 binds to the 3' UTR of Smad7 mRNA and inhibits its translation, rather than causing its degradation. Most importantly, Smad 7 is bound to Smad 2 and 3, which are thought to competitively bind to TGFBR1, and prevents their activation upon TGF-β1 stimulation. The depletion of miR-21 or the overexpression of Smad 7 blocks TGF-β1-induced CAF formation, whereas the overexpression of miR-21 or the depletion of Smad 7 promotes CAF formation, even without TGF-β1 stimulation. Collectively, these findings clearly demonstrate that miR-21 and Smad7 are critical regulators of TGF-β1 signaling during the induction of CAF formation.
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Cites
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Cited by
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Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer
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Self-citationCarcinoma-associated fibroblasts: orchestrating the composition of malignancy
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Regulation of TGF-β Family Signaling by Inhibitory Smads
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Metadata
- Authors
- Li, Q., Zhang, D., Wang, Y., Sun, P., Hou, X., Larner, J., Xiong, W., & Mi, J.
- Venue
- Scientific Reports
- Published
- 2013-06-20
- Volume
- 3
- Issue
- 1
- Pages
- 2038-2038
- ISSN
- 2045-2322 (ISSN-L)
- OpenAlex
- W2135452173
- Cited by
- 176
- References
- 15
- FWCI
- 6.32
- Type
- journal article
- Language
- en
- Open access
- gold
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