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Title, Alexandra C; Hong, Sue-Jean; Pires, Nuno D; Hasenöhrl, Lynn; Godbersen, Svenja; Stokar-Regenscheit, Nadine; Bartel, David P; Stoffel, Markus
Nature communications, 11/2018, Letnik: 9, Številka: 1Journal Article
The epithelial-to-mesenchymal transition (EMT) is an important mechanism for cancer progression and metastasis. Numerous in vitro and tumor-profiling studies point to the miR-200-Zeb1 axis as crucial in regulating this process, yet in vivo studies involving its regulation within a physiological context are lacking. Here, we show that miR-200 ablation in the Rip-Tag2 insulinoma mouse model induces beta-cell dedifferentiation, initiates an EMT expression program, and promotes tumor invasion. Strikingly, disrupting the miR-200 sites of the endogenous Zeb1 locus causes a similar phenotype. Reexpressing members of the miR-200 superfamily in vitro reveals that the miR-200c family and not the co-expressed and closely related miR-141 family is responsible for regulation of Zeb1 and EMT. Our results thus show that disrupting the in vivo regulation of Zeb1 by miR-200c is sufficient to drive EMT, thus highlighting the importance of this axis in tumor progression and invasion and its potential as a therapeutic target.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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