| First Author | Wang L | Year | 2018 |
| Journal | Elife | Volume | 7 |
| PubMed ID | 30543324 | Mgi Jnum | J:295091 |
| Mgi Id | MGI:6459633 | Doi | 10.7554/eLife.39479 |
| Citation | Wang L, et al. (2018) miR-34a is a microRNA safeguard for Citrobacter-induced inflammatory colon oncogenesis. Elife 7:e39479 |
| abstractText | Inflammation often induces regeneration to repair the tissue damage. However, chronic inflammation can transform temporary hyperplasia into a fertile ground for tumorigenesis. Here, we demonstrate that the microRNA miR-34a acts as a central safeguard to protect the inflammatory stem cell niche and reparative regeneration. Although playing little role in regular homeostasis, miR-34a deficiency leads to colon tumorigenesis after Citrobacter rodentium infection. miR-34a targets both immune and epithelial cells to restrain inflammation-induced stem cell proliferation. miR-34a targets Interleukin six receptor (IL-6R) and Interleukin 23 receptor (IL-23R) to suppress T helper 17 (Th17) cell differentiation and expansion, targets chemokine CCL22 to hinder Th17 cell recruitment to the colon epithelium, and targets an orphan receptor Interleukin 17 receptor D (IL-17RD) to inhibit IL-17-induced stem cell proliferation. Our study highlights the importance of microRNAs in protecting the stem cell niche during inflammation despite their lack of function in regular tissue homeostasis. |
