| First Author | Myant KB | Year | 2013 |
| Journal | Cell Stem Cell | Volume | 12 |
| Issue | 6 | Pages | 761-73 |
| PubMed ID | 23665120 | Mgi Jnum | J:198485 |
| Mgi Id | MGI:5496930 | Doi | 10.1016/j.stem.2013.04.006 |
| Citation | Myant KB, et al. (2013) ROS Production and NF-kappaB Activation Triggered by RAC1 Facilitate WNT-Driven Intestinal Stem Cell Proliferation and Colorectal Cancer Initiation. Cell Stem Cell 12(6):761-73 |
| abstractText | The Adenomatous Polyposis Coli (APC) gene is mutated in the majority of colorectal cancers (CRCs). Loss of APC leads to constitutively active WNT signaling, hyperproliferation, and tumorigenesis. Identification of pathways that facilitate tumorigenesis after APC loss is important for therapeutic development. Here, we show that RAC1 is a critical mediator of tumorigenesis after APC loss. We find that RAC1 is required for expansion of the LGR5 intestinal stem cell (ISC) signature, progenitor hyperproliferation, and transformation. Mechanistically, RAC1-driven ROS and NF-kappaB signaling mediate these processes. Together, these data highlight that ROS production and NF-kappaB activation triggered by RAC1 are critical events in CRC initiation. |
